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Cardiovascular Disease and Dentistry¹

DR JEE-YUN LEUNG

Learning Outcomes²

PART 1

1. Review common vascular, valvular, electrical, muscular and congenital cardiac conditions and their management (e.g. hypertension, coronary artery disease, rheumatic heart disease, infective endocarditis, arrhythmias, congenital structural defects, heart failure)
2. Describe potential oral findings associated with cardiac conditions
3. Describe the oral manifestations and manage the risks associated with common treatments used to manage cardiac conditions

• Understand the classification of cardiac conditions and their dental implications.
• Identify risk factors, manifestations, and management strategies for hypertension and ischaemic heart disease.
• Recognize the relationship between oral health and conditions such as infective endocarditis and rheumatic heart disease.
• Manage dental treatment for patients with electrical dysrhythmias and cardiac electronic devices.

4. Assess the associated risks of common dental procedures and modify dental treatment appropriately to safely provide care

PART 2

5. Work a patient up prior to cardiac surgery
6. Manage angina or an acute coronary syndrome in dental practice

• Evaluate the risks and benefits of preoperative dental treatment for patients undergoing cardiac surgery.

Classification of Cardiac Conditions³⁴

COMMON CARDIAC CONDITIONS

Hypertension, Coronary Artery Disease, Rheumatic Heart Disease, Infective Endocarditis, Arrhytmias, Congenital Structural Defects, Heart Failure

WHO INTERNATIONAL CLASSIFICATION OF DISEASES - 11TH REVISION

11 Diseases of the circulatory system

• Hypertensive diseases
• Hypotension
• Ischaemic heart diseases
• Diseases of coronary artery
• Pulmonary heart disease or diseases of pulmonary circulation
• Pericarditis
• Acute or subacute endocarditis
• Heart valve diseases
• BC20 Chronic rheumatic heart diseases, not elsewhere classified
• Diseases of the myocardium or cardiac chambers
• Cardiac arrhythmia
• Heart failure
• Diseases of arteries or arterioles
• Diseases of veins

Disorders of lymphatic vessels or lymph nodes Postprocedural disorders of circulatory system Neoplasms of the circulatory system Developmental anomalies of the circulatory system Infections of the circulatory system Symptoms, signs or clinical findings of the circulatory system Cerebrovascular diseases Functional vascular disorders of the skin JB64.4 Diseases of the circulatory system complicating pregnancy, childbirth or the puerperium

BE2Y Other specified diseases of the circulatory system BE2Z Diseases of the circulatory system, unspecified

Types of Cardiac Conditions⁵

Vascular / Ischaemic

• Hypertension
• Hypotension
• Ischaemic heart disease (Coronary artery disease) – angina, myocardial infarction
• Thromboembolic complications of CVD

Valvular

• Rheumatic fever and Rheumatic heart disease
• Infective endocarditis
• Aortic and mitral valve stenosis, regurgitation and prolapse

Electrical (Dysrhythmias)

• Extrasystoles (ectopics)
• Tachycardia (including Atrial fibrillati
  • Disturbances in heart rate or rhythm, such as atrial fibrillation.on)
• Bradycardias

Muscular (cardiomyopathies)

• Primary – genetic/inherited, acquired
• Secondary
  • Diseases of the heart muscle affecting pumping ability.

Congenital

• Cyanotic
• Acyanotic
  • Structural defects present from birth.

Heart Failure

Definition

Structural or functional impairment where blood output is insufficient for body demands.

Vascular and Ischaemic Conditions⁶

• Hypotension
• Hypertension
• Ischaemic heart disease (Coronary artery disease) – angina, myocardial infarction
• Thromboembolic complications of CVD

Hypotension Definitions and Aetiology⁷

• Hypotension (chronic arterial hypotension) = systolic BP <100 mmHg
• Pre-syncope (“near-fainting”) = condition in which a patient feels syncope is imminent
• Syncope (“fainting”) = acute fall in blood pressure, resulting in transient global cerebral hypoperfusion, causing a loss of consciousness which usually leads to loss of postural tone and falling
• Vasovagal syncope = reaction to pain, or to anxiety and fear before, during or after a dental procedure
• Orthostatic hypotension = fall in blood pressure when standing up after sitting or lying down for an extended period of time in the dental chair

Causes⁸

• Cardiac conditions: ability for heart to pump blood (e.g. abnormal heart rhythm, heart failure, MI)
• Autonomic nervous system: involved in returning BP to normal (e.g. Parkinson’s disease)
• Long-term bed rest (e.g. hospitalised, pregnancy)
• Low blood volume (e.g. dehydration, anaemia, injury)
• Medications (e.g. antihypertensives, antidepressants)

Table 5.12 Causes of orthostatic hypotension

Primary autonomic causes	Secondary autonomic causes	Non-autonomic causes
Familial dysautonomia (Riley-Day syndrome)	B vitamin deficiency	Hypovolaemia
Pure autonomic failure (idiopathic orthostatic hypotension)	Alcoholism	Ageing
Shy-Drager syndrome	Diabetes	Prolonged bed rest
Dopamine beta-hydroxylase deficiency	Parkinsonism	Pregnancy
	Porphyrin	Drugs (e.g. antihypertensives)

Scully C. Scully’s medical problems in dentistry. 7th ed. Edinburgh: Churchill Livingstone/Elsevier; 2014

General Manifestations⁹

• Early symptoms: vertigo, dizziness, visual blurring, headache, syncope
• Later: tachycardia, paleness, cold extremities, sweating

Postural Hypotension

In supine position blood volume is uniformly distributed throughout the organism. The transition from supine position to standing causes:

• redistribution of 300-800 ml of blood volume to the lower limbs and the splanchnic circulation
• BP reduction above the heart

Physiological condition: Compensatory mechanisms (vascular tone and HR increase) restore BP values

Orthostatic hypotension: Failure of compensatory mechanisms causes BP decrease

General Management of Hypotension

Syncope – patient with sudden loss of consciousness and tone¹⁰

• falls to floor
• may have brief twitching or jerking (may appear similar to an epileptic seizure, but much shorter duration)

Stop dental treatment. If the patient is in the dental chair, tilt it to be horizontal. Provide basic life support.

• If a patient does not respond, raise their legs and call for emergency help.

Has the patient regained alertness (without drowsiness or confusion) within 2 minutes [NB1]?

NO:

• Call 000 if not already in contact.
• Provide basic life support if required.
• Consider other diagnoses [NB1].
• Maintain treatment as advised by the 000 operator until the patient regains consciousness or assistance arrives.

YES:

• Keep the patient recumbent and supervised until the symptoms are fully resolved.
• Before discharging the patient:
  • check that the patient can stand unassisted without symptoms returning
  • consider referring for or seeking medical advice if the patient:
    • is an older person
    • lost consciousness while lying down or seated
    • recovers slowly
    • has recurrent episodes
    • had no obvious trigger for the fainting or near-fainting (e.g. pain, anxiety, getting up quickly after prolonged reclining)
• Advise the patient not to drive or leave the practice unaccompanied.

Presyncope – patient who feels faint or light-headed and may also have

• nausea
• anxiety
• pallor
• sweating
• tinnitus

Stop dental treatment. Tilt the dental chair to horizontal or ask the patient to lie (not sit) down. Raise the patient’s legs. Place pregnant patients onto their left side. Monitor consciousness by talking to the patient.

Does recovery occur rapidly?

YES:

• Keep the patient recumbent and supervised until the symptoms are fully resolved.
• Before discharging the patient:
  • check that the patient can stand unassisted without symptoms returning
  • consider referring for or seeking medical advice if the patient:
    • is an older person
    • lost consciousness while lying down or seated
    • recovers slowly
    • has recurrent episodes
    • had no obvious trigger for the fainting or near-fainting (e.g. pain, anxiety, getting up quickly after prolonged reclining)
• Advise the patient not to drive or leave the practice unaccompanied.

NO:

• Call 000 if not already in contact.
• Provide basic life support if required.
• Consider other diagnoses [NB1].
• Maintain treatment as advised by the 000 operator until the patient regains consciousness or assistance arrives.

NB1: Many people with chest pain do not have angina or a heart attack, but anyone with acute chest pain requires rapid medical evaluation for potentially life-threatening causes. The likelihood of angina or heart attack increases with the number of suggestive features.

NB2: Sublingual glyceryl trinitrate (GTN) dosing is a 400 microgram spray (or 300 to 600 microgram tablet) generally administered every 5 minutes to a maximum of 3 doses. Ask patients who use GTN to bring their GTN to their dental appointment so that it can be administered if chest pain occurs.

NB3: If symptoms (pain or other features that may indicate angina) last longer than the patient’s usual angina symptoms, urgent medical evaluation of a possible heart attack or other urgent condition is required.

Hypertension Classification and Aetiology¹¹

Essential (primary) hypertension (95%): High blood pressure for which a secondary cause cannot be found.

Secondary hypertension (5%): Systolic BP >140mmHg and diastolic BP >90mmHg with an identifiable cause.

National Heart Foundation of Australia – Classification of Blood Pressure¹²

Diagnostic category*	Systolic (mmHg)	Diastolic (mmHg)
Optimal	<120 and <80	-
Normal	120–129 and/or 80–84	-
High-normal	130–139 and/or 85–89	-
Grade 1 (mild) hypertension	140–159 and/or 90–99	-
Grade 2 (moderate) hypertension	160–179 and/or 100–109	-
Grade 3 (severe) hypertension	≥180 and/or ≥110	-
Isolated systolic hypertension	>140 and <90	-

*When a patient’s systolic and diastolic blood pressure levels fall into different categories, the higher diagnostic category and recommended actions apply.

Essential Hypertension¹³

• Genetic predisposition
• High basal metabolic index
• Sympathetic overactivity (40% have raised catecholamines and noradrenaline)
• High alcohol, salt intake

Secondary Hypertension

• Renal disease (80%)
• Endocrine conditions: pregnancy, Cushing syndrome, corticosteroids, hyperaldosteronism, acromegaly
• Cerebral disease: cerebral oedema (mainly strokes, head injuries or tumours)
• Coarctation of aorta
• Sleep apnoea
• Drugs: oral contraceptive pill, HRT, corticosteroids, NSAIDs, sympathomimetics (decongestants, diet pills, cocaine), stimulants (amphetamine), cyclosporine / tacrolimus, excess alcohol, SNRIs and MAOIs, haemopoietic drugs

Epidemiology¹⁴

• Australian Institute of Health and Welfare
• 39% of Australians >18yo have hypertension (~7.2 million adults)
• Of adults with hypertension:
  • 80-82% of those <54yo had uncontrolled hypertension
  • 65% had been dispensed antihypertensive medications
• Hypertensive disease contributed to 13% of all Australian deaths in 2023
• Hypertension is disproportionately high in First Nations adults.
• Nearly 1 in 20 (5%) Australian women aged 15-44 giving birth had new onset hypertension in pregnancy
• 24% of ATSI adults >18yo had hypertension 2022-2023
• Source: https://www.aihw.gov.au/reports/risk-factors/hypertension/contents/summary

Primary	Complications
Usually asymptomatic	Arteriosclerosis
Advanced cases: headache, blurred vision, tinnitus, fatigue, dizziness, angina	Cerebrovascular disease (stroke)
	Peripheral vascular disease
	Hypertensive retinopathy
	Hypertensive heart disease
	Hypertensive renal disease
	Hypertensive crisis

Clinical Manifestations

The disease itself has few oral manifestations, with the exception of facial palsy during a hypertensive crisis.

General Management of Hypertension¹⁵¹⁶

• Identify and manage risk factors: physical activity, smoking cessation, weight control, diet, alcohol intake, etc.
• Assess presence/absence of organ damage
• Pharmacologic strategies: most widely used first-line ACEIs and ARBs

FIGURE 6.1 Treatment strategy for patients with newly diagnosed hypertension

Source: https://www.heartfoundation.org.au/for-professionals/hypertension

Effective Drug Combinations¹⁷

First drug	Second drug	Comment
Effective combination
ACE inhibitor or ARB*	plus Calcium channel blocker	Particularly useful in presence of diabetes and/or lipid abnormalities1,24
ACE inhibitor or ARB*	plus Thiazide diuretic	Useful in presence of heart failure or post stroke
ACE inhibitor or ARB*	plus Beta-blocker	Recommended post myocardial infarction or in patients with heart failure2
Beta-blocker	plus Dihydropyridine calcium channel blocker	Useful in presence of symptomatic coronary heart disease
Thiazide diuretic	plus Calcium channel blocker
Thiazide diuretic	plus Beta-blocker	Not recommended in presence of glucose intolerance, metabolic syndrome or established diabetes
Combinations to use with care
Diltiazem	plus Beta-blocker	Due to risk of heart block, but risk is less than with verapamil
ACE inhibitor or ARB	plus Potassium-sparing diuretic	Due to risk of hyperkalaemia
Combinations to avoid
ACE inhibitor	plus ARB	Increased risk of renal dysfunction1,20
Verapamil	plus Beta-blocker	Due to risk of heart block

• ACE, angiotensin-converting enzyme; ARB, angiotensin receptor blocker a In head-to-head trials ACE inhibitors and ARB’s are equally effective in blood pressure reduction and prevention of cardiovascular events overall, however may have important differences in their efficacy, so that they are not interchangeable, in some clinical conditions.

• Carvedol; bisoprolol (beta-1 selective antagonist); metoprolol extended release (beta-1 selective antagonist); nebivolol.

Antihypertensive Drug Treatment – Manage Associated Conditions

1. Starting drug treatment: Start with low-moderate recommended dose of a first-line drug. If not well tolerated, change to a different drug class, again starting with a low-moderate recommended dose.
2. If target not reached after 3 months: Add a second drug from a different pharmacological class at a low-moderate dose, rather than increasing the dose of the first drug. This maximizes antihypertensive efficacy, while minimising adverse effects.
3. If target not reached after 3 months: If both antihypertensive drugs have been well tolerated, increase the dose of one drug (excluding thiazide diuretic) incrementally to the maximal recommended dose before increasing the dose of the other drug.
4. If target not reached after 3 months: If, despite maximal doses of at least two drugs, a third drug class may be started at a low-moderate dose. It is advisable to reassess for non-adherence, secondary hypertension and hypertension effects of other drugs, treatment resistant state due to sleep apnoea, underdosed use of alcohol or recreational drugs or high salt intake.
5. If blood pressure remains elevated, consider seeking specialist advice.

*Maximum effect of drug likely to be seen in 4-6 weeks. If baseline blood pressure is severely elevated earlier recess may be considered. For steps 1-4, review every 4-6 weeks for tolerance, efficacy and adverse effects. TAD patients should receive intensive advice with follow-up based on clinical context.

Drug Class	Examples	Oral Side Effects
ACEI	Captopril, Ramipril	Burning mouth syndrome, angioedema, ulceration, dysguesia, dry mouth, lichenoid reactions, coughing, taste disturbances
ARB	Candesartan, Irbesartan, Losartan, Valsartan	Facial flushing, taste disturbances, dry mouth, increased gag reflex, lupoid reactions
β-adrenergic blockers	β₁ selective (not bronchioles): Atenolol, Bisoprolol, Metoprolol; Non-selective: Propranolol	Dry mouth, lichenoid lesions, paraesthesia, taste changes
Calcium channel blockers	Dihydropyridines (vascular selective): Amlodipine, Nifedipine, Nicardipine; Non-dihydropyridines (heart rate lowering): Phenylalkylamine class: Verapamil, Gallopamil; Benzothiazepine class: Diltiazem	Gingival hyperplasia (dihydropyridines), angioedema, facial flushing, xerostomia, metallic taste (diltiazem)
Diuretics	Hydrochlorothiazide, Furosemide, Spironolactone	Dry mouth

Oral Management of Hypertensive Patients¹⁸¹⁹

• General dental treatment possible if blood pressure is controlled
• Drug interactions and side effects
• Decrease endogenous catecholamine release: dental anxiety, “white coat syndrome”, manage pain
• Underlying disease or problems (cardiac/renal/endocrine)
• Avoid elective dental treatment if >180/110 mmHg → refer for medical assessment
• Anaesthetic and sedation risks:

BP (Systolic/Diastolic)	Stage	ASA Grade
<140 and <90	-	I
140-159 and 90-99	1 Borderline/Mild	II
160-179 and 95-109	2 Moderate	III
>180 and >110	3 Severe	IV

Risk factor when evaluating peri-procedural bleeding risk (Therapeutic Guidelines v4 2026 – Figure 13.73)

Is the dental PROCEDURE likely to cause prolonged bleeding (see this table classifying procedural bleeding risk)?

• YES
• NO → Treat using approach in this table

Does the patient have any of the following MEDICAL CONDITIONS?

• a medical condition affecting haemostasis

• signs of bleeding, bruising or purpura

• a personal or family history of prolonged bleeding after dental or other procedures

• YES → Ask the medical practitioner or team for details of the medical history to clarify patient risk factors and ways to modify them (including review of medications). Create a management plan. Consider consultation with a specialist medical or dental team. Consider:

  • the level of risk
  • the treatment setting and access to specific haemostatic measures
  • access to after-hours care, especially for rural and remote patients.
  • Referral may be appropriate for higher-risk procedures or conditions requiring measures outside the practitioner’s skill set.

• NO

Is the patient taking an ANTITHROMBOTIC DRUG (including over-the-counter aspirin)?

• YES → Is the anticoagulation drug for long-term (indefinite) use?
  • YES → Does the patient have AN ADDITIONAL FACTOR that heightens risk in conjunction with an antithrombotic, such as:
    • uncontrolled hypertension (e.g. systolic blood pressure more than 160 mmHg)
    • suboptimal anticoagulation control (e.g. fluctuating or high INR)
    • age older than 65 years or frailty
    • other medication that can impair haemostasis?
    • NO
  • NO → Manage according to the type of antithrombotic drug being used (see advice on management of antithrombotics). Seek advice from a medical practitioner or a specialist dental team if uncertain about assessing or managing bleeding risk.
• NO → Is the patient taking any other medication that can impair haemostasis?
  • YES → See advice for patients taking other medications.
  • NO → Treat with standard approach.

Access²⁰

• Timing / Appointments: Short, minimally stressful, ideally late morning
  • Late morning appointments are preferred to avoid early morning catecholamine peaks.
• Positioning: orthostatic hypotension (ACEIs, ARBs)
• Setting: hospital if severe/uncontrolled hypertension and urgent dental care needed

Education / Prevention

• Common risk factor approach: smoking, alcohol, diet
• Antihypertensives: dry mouth management
• Calcium channel blockers (e.g. amlodipine) → gingiva enlargement
  • Minimise with good oral hygiene and perio debridement - Emphasize oral hygiene to mitigate drug-induced hyperplasia.
  • Extensive enlargement → specialist periodontal and medical management

Surgery²¹

• Check BP control prior to treatment
• Manage dental anxiety (exacerbates hypertension)
• Avoid NSAIDs = diuretic + either of:
  • Angiotensin converting enzyme inhibitor (e.g. perindopril)
  • Angiotensin II receptor blocker (e.g. candesartan)
  • → risk of acute kidney injury
• Sedation may be helpful to control stress/blood pressure
  • Pending nature and severity of underlying disease

Vasoconstrictors and Local Anaesthesia in Hypertension²²²³

How Much Adrenaline-Containing LA Can We Use?²⁴

• Profound anaesthesia for pain and anxiety control is important to ↓ endogenous catecholamine release

• LA with adrenaline:

  • Delays systemic absorption
  • Increases duration of anaesthesia
  • Provides local haemostasis
  • Reduces the dose required

• Poses a theoretical risk:

  • Stimulates α and β adrenergic receptors (tachycardia, increase BP)
  • Irritates cardiac pacemaker cells (arrhythmias)

• Evidence regarding maximum safe dose of adrenaline is lacking

• Malamed 2004: Most frequently quoted. Recommended max 0.04mg adrenaline per dental appt.

  • ~2 cartridges containing 1:100,000 adr (0.018mg per 1.8ml cartridge, or 0.022mg per 2.2ml cartridge).

• Tolas et al 1982, Cioffi et al 1985: Evaluated healthy pts following 2% lignocaine 1:100,000 adr injection

  • After 1.8ml (1 cartridge): plasma levels incr 2-3x, no signif changes in BP or HR
  • After 5.4ml (3 cartridges): plasma levels incr 5-6x, signif incr HR and BP

• Godzieba et al 2014: systematic review of 11 RCTs

  • Use of ≤4 cartridges of lignocaine with 1:100,000 adrenaline seems relatively safe for cardiovascular compromised patients

• Serrera Figallo et al 2012: systematic review of RCTs

  • Possible to use a dose between 1.8ml and 3.6ml on a general basis in patients with CVD

• Conclusion:

  • Use of >2 cartridges of vasoconstrictor-containing LA should be considered a relative rather than absolute contraindication.
  • Current consensus seems to favour judicious use of local anaesthetics containing vasoconstrictors to ensure profound anaesthesia

Recommendations²⁵

• If supplementation with plain LA is required, use vasoconstricting LA first
• Aspirating syringe
• Intraligamentary injection contraindicated
• Some report felypressin has fewer haemodynamic effects
  • Felypressin is a safe alternative with minimal myocardial effects.
• ?Adrenaline-containing retraction cord astringent

Therapeutic Guidelines v4 2026

• Local anaesthetics containing adrenaline = limited effect on BP elevation
• Avoid in patients with uncontrolled hypertension
• Consider felypressin (Citanest® = prilocaine + felypressin)
• Also avoid: MI in previous 6 months, unstable angina, uncontrolled arrhythmias, uncontrolled hyperthyroidism

Ischaemic Heart Disease Definition and Aetiology^26272829

• Definition: Group of syndromes resulting from myocardial ischaemia – an imbalance between cardiac blood supply (perfusion) and myocardial oxygen demand.
• Classification / Aetiology:
  • Stable angina: chronic symptoms
    • Stable atherosclerotic plaque → Fixed coronary obstruction
  • ACS: new or increasing ischaemic symptoms
    • Unstable atherosclerotic plaque or endothelial disruption → transient/permanent thrombotic occlusion → ischemia and infarction

Classification / Aetiology³⁰

Figure 3.2 Classification of coronary ischaemic syndromes

Coronary Ischaemic Syndromes
Stable Angina	Acute Coronary Syndromes
	STEMI
	NSTEMI

NSTEACS = non–ST elevation acute coronary syndrome; NSTEMI = non–ST elevation myocardial infarction; STEMI = ST elevation myocardial infarction.

NB1: NSTEACS can progress to STEMI and acute coronary occlusion can occur without ST elevation, so ongoing monitoring is essential.

Acute coronary syndromes

• Non-ST elevation acute coronary syndrome
  • Unstable angina = without elevated cardiac biomarkers
  • Non-ST elevation myocardial infarction = pts with MI as determined by elevated cardiac biomarkers
• ST-elevation myocardial infarction = medical emergency
  • NSTEACS can progress to STEMI

Thygesen K, Alpert JS, Jaffe AS, Chaitman BR, Bax JJ, Morrow DA, et al. Fourth Universal Definition of Myocardial Infarction (2018). J Am Coll Cardiol 2018;72(18):2231-64

1) Type 1 myocardial infarction: 1. Atherothrombotic coronary occlusion compromises myocardial blood flow

2) Type 2 myocardial infarction: 1. Secondary to an imbalance between myocardial oxygen supply and demand (arises from e.g. tachyarrhythmias, sustained bradyarrhythmias, anaemia, respiratory failure and hypotension) 2. Coronary artery spasm 3. Spontaneous coronary artery dissection 4. Coronary embolism

Risk Factor	Description
H	Heredity
A	Age (older)
S	Sex (male)
L	Lipidaemia
I	Increased weight (obesity)
P	Pressure (arterial hypertension)
I	Inactivity (sedentary lifestyle)
D	Diabetes
S	Smoking tobacco

Dr Jee-Yun Leung

Epidemiology:

• Leading cause of death globally: 13%
• Prevalence: 3% in Australia (higher amongst males)
• Significant decrease in age-standardised IHD mortality rates
  • 1960s: 7/10 MI’s fatal ; Today: 7/10 survive a MI
• CVD-related prescriptions increased 7-8 fold in this time

General Manifestations of Ischaemic Heart Disease³¹³²³³

Figure 13.81 Probability that chest pain is ischaemic in origin based on common descriptions of pain

High Probability of Ischaemia	Moderate Probability	Low Probability
pressure		sharp
squeezing		fleeting
gripping		shifting
heaviness		pleuritic
tightness		positional
exertional or stress-related
retrosternal
left-sided
dull
aching
stabbing
right-sided
tearing
ripping
burning

Source: Gulati M, Levy PD, Mukherjee D, Amsterdam E, Bhatt DL, Birtcher KK, et al. 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR Guideline for the Evaluation and Diagnosis of Chest Pain: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation 2021;144(22):e368-e454.

Stable Angina	Acute Coronary Syndromes (e.g. MI)	Cardiac Arrest
• Episodic retrosternal chest discomfort (pain, ache or tightness)	• “Crushing” or heavy central chest pain (more severe)	• Sudden loss of consciousness
• May radiate to arms, neck, back, shoulder, jaw	• Shortness of breath, nausea, sweating, pale/clammy skin	• No pulse
• Commonly triggered by physical activity or emotional stress	• Decrease pulse & BP, vomiting, “impending sense of doom”	• Not breathing
• Predictable, consistent over time	• May occur at rest
• Lasts <10min if provoking stimulus removed	• Lasts 20min to hours
• Subsides with rest or GTN	• Not relieved by rest or GTN
	• NB: Silent Angina = some may have no pain due to psychological factors persistently inhibiting pain perception (elderly) or autonomic neuropathy (diabetics)

Ischaemic Heart Disease: General Management³⁴

Lifestyle	Pharmacological	Revascularisation
• ↓ Smoking	• Beta-blockers	• Coronary artery bypass grafting (CABG)
• Diet	• Calcium-channel blockers	• Percutaneous coronary intervention (PCI) = “coronary angioplasty and stent”
• ↓ Alcohol	• Nitrates
• Physical Activity	• Nicorandil
• Healthy weight	• ACE inhibitors
• Psychosocial	• ARBs
	• Antiplatelets
	• Lipid-lowering drugs
	• Ivabradine

Therapeutic goal	Pharmacological strategy
Inhibit progression atherosclerosis	Statins - ↓lipids
↑coronary circulation	Nitrates, Ca channel blockers
↓heart workload	B blockers
Prevent thrombus formation	Anti-thrombotic agents

Oral Manifestations of Ischaemic Heart Disease³⁵

• Antihypertensive drugs: as per previous section
• Nicorandil: oral/skin/eye ulceration, facial flushing, lupoid lesions
• Possible association with periodontitis (growing evidence)
  • Direct pathway – bacteraemia
  • Indirect pathway – induces chronic systemic inflammatory state
• Possible association with endodontic disease (less investigated and inconclusive evidence)
  • apical periodontitis – comparable inflammatory and microbial profile (gram –ve anaerobes) to periodontal disease
  • pulp stones – similarity to calcified stones forming in coronary and renal arteries
• Rarely, angina pain referred to lower jaw/teeth mistakenly thought to be of dental origin (clue: onset with exertion)

Periodontitis and Atherosclerotic Cardiovascular Disease³⁶

Category	Details
Journal	Circulation
Author	Andrew H. Tran, MD, MPH, MS, FAHA, Chair; Abbas H. Zaidi, MD, MS, Vice Chair; Ann F. Bolger, MD, FAHA; Oscar H. Del Brutto, MD, Rashmi Hegde, BDS, MS, Lauren L. Patton, DDS, Jamie Rausch, PhD, RN, and Justin P. Zachariah, MD, PhD, FAHA on behalf of the American Heart Association Cardiovascular Disease Prevention Committee
Publish	Volume 153, Number 6

Atherosclerotic cardiovascular diseases (ACVDs) are a leading cause of death and disability across the developed world and impose a vast burden on healthcare resources. This category of diseases includes:

• Coronary heart disease, which presents as angina or heart attack (myocardial infarction).
• Ischaemic cerebrovascular disease, which may manifest as stroke or mini-stroke (transient ischaemic attack or TIA).
• Peripheral vascular disease.

Periodontitis, although not a cause of mortality, is also a major public health concern because of its high prevalence in the population and its negative impact on oral health, ability to chew, appearance, quality of life, dental care costs and tooth loss. In addition, as a progressive, chronic inflammatory disease, untreated periodontitis has the potential to undermine overall health and even exacerbate other inflammatory conditions, such as ACVD.

European Federation of Periodontology: https://www.bsperio.org.uk/assets/downloads/EFP_cardiovascular-disease-gum-disease.pdf

Dental Management of Ischaemic Heart Disease³⁷³⁸

Careful medical history at first appointment. Ask about indicators of risk:

• History of chest pain at rest
• Triggers/frequency of episodes
• Carry GTN?
• How episodes are usually managed
• Number of anti-anginal medications
• Hx of CABG/stent placement with ongoing symptoms
• Hx of heart failure

Timing	Angina	Prior to cardiac surgery	After MI or Cardiac Surgery
Risk of Vascular Events	Appropriate setting	Emergency Management	Adrenaline
Drug Therapy	Anxiety management	Periodontitis
?Endodontics	Apical Periodontitis	Dental Pulp Stones
	Antihypertensive drugs	Antiplatelet drugs	Lipid-lowering drugs

Access³⁹

• Access to clinic / Mobility: Functional capacity (cardiopulmonary reserve)
• Appointments: Short, minimally stressful appointments. Late morning appointments.
• Positioning: Orthostatic hypotension (antihypertensives) → semi-supine and slowly upright
• Location / setting: Hospital setting may be required for severe cardiac disease when emergency dental treatment required.
• Timing:
  • Patients with history of angina (or MI >6 months earlier) can undergo dental treatment if medically stable
  • Defer elective dental care if unstable angina
  • Defer elective dental procedures for 6 months after MI, stent placement or CABG.
  • Pain and infection within 6 months of above:
    • provide adequate emergency treatment
    • avoid use of adrenaline-containing LA
    • consider specialist advice re: appropriate treatment and timing of procedures

Capacity⁴⁰

• Nil significant

Consent

• Nil significant

Education/Prevention

• Oral side effects of medications
• Possible association with periodontitis +/- endodontic disease

Surgery⁴¹

Pre-operative

• Instruct patients with angina to bring their medication (e.g. GTN spray or tablets), and have it readily accessible.
• Ensure GTN and oxygen readily available
• Monitor SpO${}_2$, BP, HR

Peri-operative

• Use relaxation techniques and consider other measures for anxiety management
• Limit the duration of dental procedures
• Bleeding: may be on antithrombotics (see Haematology – Bleeding Disorders lecture)
• LA: Ensure effective analgesia → use of adrenaline (see Hypertension)
  • Limit adrenaline-containing local anaesthetic to a maximum of 2 cartridges.
• Sedation: anxiety relief helpful (see Hypertension)

Medication Safety

Avoid NSAIDs in patients taking a “triple whammy” (diuretic + ACE inhibitor/ARB + NSAID) due to the high risk of acute kidney injury. Uncontrolled hypertension (systolic >160 mmHg) is a risk factor for increased bleeding, especially in patients taking antithrombotics.

Post-operative

• Caution with NSAIDs

Management of Chest Pain in Dental Practice⁴²

NB1: Many people with chest pain do not have angina or a heart attack, but anyone with acute chest pain requires rapid medical evaluation for potentially life-threatening causes. The likelihood of angina or heart attack increases with the number of suggestive features.

NB2: Sublingual glyceryl trinitrate (GTN) dosing is a 400 microgram spray (or 300 to 600 microgram tablet) generally administered every 5 minutes to a maximum of 3 doses. Ask patients who use GTN to bring their GTN to their dental appointment so that it can be administered if chest pain occurs.

NB3: If symptoms (pain or other features that may indicate angina) last longer than the patient’s usual angina symptoms, urgent medical evaluation of a possible heart attack or other urgent condition is required.

Management of chest pain in dental practice⁴³

Patient with chest pain and any of the following features suggestive of heart attack [NB1]:

• a prior diagnosis of angina or heart attack, or chest pain on exertion
• persistent central chest sensation of: pressure, squeezing, gripping, heaviness, or tightness
• radiation of the pain, pressure or tightness to the arms, neck, back or jaw
• breathlessness, nausea, vomiting, sweating or fatigue (these can be present in angina or heart attack without pain, especially in older patients, females and people with diabetes).

NO → Call 000.

• Give oxygen by face mask if either:
  • the patient is breathless or looks blue
  • the pulse oximeter reading is less than 94% (if pulse oximetry is available).
• Give 300 mg oral aspirin (non-enteric coated) if available, to chew or dissolve (unless the patient has a known aspirin allergy).
• Recline the patient within their comfort range.
• Have defibrillator ready; prepare for basic life support.

YES → Recline patient within their comfort range.

• Administer sublingual GTN doses at intervals according to the patient’s usual regimen [NB2].
• Are the symptoms (pain or other features) persisting for longer than the patient usually experiences them [NB3]?
  • YES → (connects back to Call 000 box as described above)
  • NO → Temporise any treatment that has been started.
    • Referral to general practitioner for review is reasonable.

If administering nitrates, recline the patient because blood pressure can be reduced by administration. To manage chest pain in a patient with a history of angina, use:

1. glyceryl trinitrate spray 400 micrograms sublingually, repeat every 5 minutes if pain persists, up to a total of 3 doses if tolerated

OR

1. glyceryl trinitrate tablet 300 to 600 micrograms sublingually, repeat every 5 minutes if pain persists, up to a total of 3 doses if tolerated.

To manage chest pain if angina or heart attack is suspected, provided no contraindication (e.g. aspirin allergy) is present, use:

• aspirin (non-enteric coated) 300 mg orally, chewed or dissolved before swallowing.

Thromboembolic Complications of Cardiovascular Disease⁴⁴

• Arterial thrombi: platelet aggregation + fibrin + erythrocytes
• Venous thrombi: slow & turbulent blood flow, ↑ risk small emboli detaching & blocking pulmonary arteries

General Manifestations⁴⁵

Arterial thrombi

• TIA/stroke
• Occlusion of coronary artery grafts
• MI & death in unstable angina
• Systemic embolism with prosthetic heart valves/AF

Venous thrombi

• DVT
• Pulmonary embolism

General management

• Antithrombotic agents: prevent thrombus formation (initiation)
• Anticoagulants: prevent coagulation (clot formation)

Dental management

• Antithrombotic drug use → bleeding (see Haematology - Bleeding Disorders lecture)

Valvular Conditions⁴⁶

• Rheumatic fever and Rheumatic heart disease
• Infective endocarditis
• Aortic and mitral valve stenosis, regurgitation and prolapse

Rheumatic Fever and Rheumatic Heart Disease⁴⁷⁴⁸

Definition⁴⁹

• Rheumatic Fever: An acute, immunologically-mediated, systemic inflammatory condition characterised by fever and arthritis 2-4 weeks after pharyngitis. Caused by certain strains of Group A beta-haemolytic streptococci (e.g. following impetigo and scabies).

Epidemiology

• 1.06 Acute rheumatic fever and rheumatic heart disease - AIHW Indigenous HPF
• RHD is a disease of disadvantage that is both preventable and treatable.
• First Nations people in Australia have one of the highest recorded rates of ARF and RHD in the world (119 per 100,000), with incidence rates increasing (50% increase 2012-2021)
• First Nations people accounted for 92% of the total number of ARF cases in Australia recorded over the 5-year period 2017–2021
• Otherwise rare disease in Western world, common in Indian subcontinent, Middle East, some Caribbean islands.

Aetiology⁵⁰

• Group A streptococci
• RHD: repeated episodes of RF
• Autoimmune reaction: antibodies produced to fight streptococci cross react with enzymes of the heart
• Antibodies against streptococci cross-react with heart valves, causing scarring and permanent damage (most commonly the mitral valve).

Figure 2 Pathophysiology of RHD. RHD occurs as a sequela of GAS infection, especially pharyngitis. Social determinants of health and genetic predisposition play a role in repeated infection as well as in the progression to RHD. Cross-reactive antibodies and immune cells form in response to GAS infection and attack endothelial cells throughout the body; however, damage to the endothelial surface of the valves is not repaired effectively.

Image: Simpson MT, et al. Rheumatic Heart Disease in the Developing World. Structural Heart. 2023; 7(6): 100219

General Manifestations⁵¹

• Acute Rheumatic Fever
• Subacute/chronic Rheumatic Fever

Acute rheumatic fever

Etiology	Previous GAS pharyngitis/tonsillitis without antibiotic treatment
Peak incidence	5–15 years of age
Diagnosis	Evidence of a previous GAS infection (e.g., throat culture, rapid antigen detection test, antistreptolysin O, antistreptococcal DNase B test) Revised Jones criteria	Constitutional High fever Malaise Fatigue	Heart Valvulitis Pancarditis
Treatment	Antibiotic treatment of underlying GAS infection Symptomatic treatment of arthritis and fever	CNS 1–8 months after infection Sydenham chorea Jerking Flinching
		Skin Erythema marginatum Subcutaneous nodules
				Joints Migratory polyarthritis

Pathophysiology and disease course

Untreated GAS pharyngitis/tonsillitis	Development of antibodies	Molecular mimicry	Type II hypersensitivity reaction	Inflammation and cell damage
Acute infection		Latent period (2~4 weeks)		Rheumatic fever onset

• Rheumatic Heart Disease
• Valvular damage → regurgitation, stenosis → IE risk
• Early heart disease: Heart murmur
• Late effects: heart enlargement, cardiac failure
• Other:
  • Shortness of breath
  • Chest pain
  • Fatigue
  • Swollen legs and feet

Diagnosis	Treatment	Prognosis
Physical examination History collection Echocardiogram Electrocardiogram Blood tests	Antibiotic prophylaxis (benzathine benzylpenicillin G) Complications: - Anticoagulants - Balloon valvuloplasty - Heart valve repair or replacement - Heart failure management - Lifestyle and prevention	- Acute phase lasts 6-12 weeks, definitive cure up to 6 months - RF recurrence rate is high (50% in first 5 years) → prophylactic therapy with penicillin - Mortality rate: 0.5 per 100,000

Infective Endocarditis⁵²

Definition⁵³

A rare, but dangerous, infection of the endocardial surface of the heart. Predominantly affects one or more heart valves, especially where there is turbulent blood flow because of valve damage (typically left sided valves).

Epidemiology

• Relatively uncommon illness with high morbidity and mortality
• 2010: Australian incidence 4.7 cases per 100 000 person-years
• In-hospital mortality variable – increases with age (up to 15% in 80-89 yos)

Aetiology⁵⁴

• Endothelial sites with turbulent blood flow
  • Platelet and fibrin deposits accumulate (non-thrombotic endocarditis)
  • sterile “vegetations” produced
  • can be readily infected if a subsequent bacteraemia occurs

Causative organisms: Streptococci viridans (oral) 50-60%, Enterococci (faecal strep) 10%, Staphylococci (skin) 20-30%, Others 10% (Gram negative bacilli – mainly HACEK group, fungi)

Association with Dentistry⁵⁵

• Dental procedures involving bleeding can initiate a bacteraemia that may lead to endocarditis (usually transient and <15min, but occasionally up to 1 hour)
• Most common types of bacteraemia in IE:
  • S mutans and S sanguis (both Strep viridans) from dental plaque [40% of IE causative organisms due to complex attachment mechanisms enabling them to adhere to endocardium]
  • Gram negative bacilli (HACEK group, including AA) occasionally implicated
• Chance of dental extraction causing IE in patient with valvular disease may be as low as 1 in 3000, therefore bacteraemia not synonymous with IE (or would need antibiotic cover for brushing).

Dental treatment is not the only source of IE-bacteraemia

Susceptible surface + high circulating bacterial loads

Risk Categories⁵⁶

High risk: previous IE, prosthetic heart valves or valves repaired with prosthetic material, unrepaired cyanotic congenital heart disease, or some repaired congenital heart defects (up to 6 months after the procedure or lifelong if residual shunt or valvular regurgitation remains), +/- cardiac transplantation with cardiac valvulopathy.

Moderate risk: previous rheumatic fever, heart murmur, or evidence of native valve disease.

Table 5.32: Main groups affected by infective endocarditis

Aetiology	Approximate % of all cases of infective endocarditis
No obvious cardiac valve disease	40
Chronic rheumatic heart disease	30
Congenital heart disease	10
Prosthetic cardiac valves	10
Intravenous drug abuse	10

Variable (flu-like) symptoms	Septic emboli (20-45%) – Systemic manifestations	Cardiac manifestations	Immune complex formation from antigens’ resultant antibodies
Fever	Infarcts brain (→ stroke), limbs, spleen (→ splenomegaly), kidney (→ haematuria), pulmonary.	Sepsis	Vasculitis
Headache	Retinal necrosis and blindness	Tachycardia	Arthritis
Joint pain	Mycotic aneurysms	Hypotension	Renal damage
Malaise	Focal glomerulonephritis	Valve destruction
SOB/cough		Murmur
Chest pain (esp IVDUs)		Pericarditis
		Coronary artery embolism

Common signs: 90% fever, 85% heart murmurs

Management Complexity

Infective endocarditis requires long-term IV antibiotics and often urgent valve replacement due to high mortality rates (15-20% during admission).

General Management⁵⁷

Treatment	Prognosis
- Hospital admission for early treatment	- 15-20% die during initial hospital admission; further 10-15% die over the following year
- Antibiotic therapy	- 40-45% require surgery during initial hospital admission; further 10% require surgery within 1 yr post-discharge
- Severe cases: valve replacement	- Good prognostic factors: young, penicillin-sensitive isolates, early tx

Aortic and Mitral Valve Disorders⁵⁸

• Aortic stenosis: narrowing of the aortic valve; this generates an increased pressure in the left ventricle to maintain the blood volume per beat
• Aortic regurgitation: blood propelled to the aorta during systole returns to the left ventricle during diastole due to a defective aortic valve
• Mitral valve stenosis: Narrowing of the mitral valve that generates an increasing pressure in the left atrium of the heart
• Mitral valve regurgitation: The blood propulsed to the left ventricle during systolic contraction returns into the left atrium during diastolic dilatation due to a valve closure defect
• Mitral valve prolapse: Protrusion of the valves into the left atrium during systole. May exist in isolation, but sometimes associated with mitral regurgitation. May be associated with atrial septal defect, patent ductus arteriosus.

→ DO NOT REQUIRE ANTIBIOTIC PROPHYLAXIS

Valve Replacement⁵⁹

• Tissue valve
  • Material: porcine, bovine, human
  • Lifespan = 10–20 years
    • Usually for older patients
  • No turbulence = no anticoagulation required
    • Unless required for other reason e.g. AF, DVT
  • No noise
• Mechanical valve
  • Material: carbon, titanium
  • Lifespan = highly durable, can last lifetime (30+ years)
    • Usually for younger patients
  • Turbulence = anticoagulation required
    • Requires lifelong warfarin due to turbulence.
  • Noisy

Dental Management of Valvular Heart Disease⁶⁰

Risk Assessment⁶¹

• Bacteraemia to heart valves
• Oral hygiene
• Timing to perform dental treatment
• Anticoagulation
• Oral side effects of diuretics (e.g., furosemide), ACE inhibitors, and beta-blockers
• GA/sedation risks: myocarditis
• Concurrent antibiotic therapy
  • Identify patients requiring antibiotic prophylaxis by referring to Therapeutic Guidelines Version 4.

Access⁶²

• Postpone elective dental care 6 months after episode of RF
• RHD → IE or valve surgery = urgent management of dental infections (bacteraemia)
  • May be hospital in-patient setting
  • IVDUs: less reliable attendance unless in pain

Capacity/Consent

• Nil significant

Education/Prevention

• Good oral hygiene most important factor in reducing risk in susceptible individuals
• Preventive measures to avoid caries and periodontal disease
  • OHI for home maintenance, regular dental attendance, diet, etc
• Patient educated to alert dental providers of RHD/IE history, and need for antibiotic prophylaxis

Surgery⁶³

• Antibiotic prophylaxis
• Liaise with Infectious Diseases physician if on concurrent antibiotics
• Consult with physician re: anticoagulation
• LA: use adrenaline with caution, aspirating syringe (IV injection may precipitate arrhythmias)
  • Liaise with physicians regarding anticoagulation management, specifically for patients on Warfarin or DOACs.
• Conscious sedation / GA: avoid when acute RF (myocarditis), hospital environment if required

Spread

• Infective endocarditis bacteraemia
• Possible antibiotic resistance issues

Table 2.5 Indications for antibiotic prophylaxis for endocarditis

Antibiotic prophylaxis against infective endocarditis is recommended only for people who meet both of the following criteria:

• are undergoing a procedure associated with a high risk of a bacteraemia and subsequent infective endocarditis
• have a cardiac condition associated with an increased risk of developing infective endocarditis and the highest risk of adverse outcomes from endocarditis.

Procedures for which endocarditis prophylaxis is recommended for patients with a cardiac condition listed below [NB1]

• Dental procedures – only those involving manipulation of the gingival or periapical tissue or perforation of the oral mucosa (eg dental extractions, implant placement, biopsy, removal of soft tissue or bone, subgingival debridement, replanting avulsed teeth) [NB2] [NB3] [12] [33] [44].

NB1: Endocarditis prophylaxis is not recommended for procedures other than those covered in this topic. However, surgical prophylaxis may be indicated even if endocarditis prophylaxis is not – see Surgical antibiotic prophylaxis recommendations for specific procedures.

NB2: For a list of dental procedures classified by invasiveness and their indications for endocarditis prophylaxis, see Table 13.29.

NB3: Evidence on the risk of bacteraemia and subsequent infective endocarditis following supra- and subgingival debridement is conflicting. Pending further evidence, endocarditis prophylaxis is only recommended for supra- and subgingival debridement that involves manipulation of the gingival tissue [49] [50].

Commentary (NB6): Endocarditis prophylaxis is not recommended for patients with forms of valvular or structural heart disease not listed in this table, including patients with mitral valve prolapse, septal defects or cardiac implantable electronic devices.

NB7: Patients with a heart transplant who have developed cardiac valvulopathy may also be at high risk of adverse outcomes from endocarditis; consult the patient’s cardiologist for specific recommendations.

Cardiac conditions for which endocarditis prophylaxis is recommended for patients undergoing a procedure listed above [NB5] [NB6]

• prosthetic cardiac valve, including transcatheter-implanted prosthesis or homograft
• prosthetic material used for cardiac valve repair, such as annuloplasty rings and chords
• previous infective endocarditis
• ventricular assist devices
• congenital heart disease but only if it involves:
  • unrepaired cyanotic defects, including palliative shunts and conduits
  • repaired defects with residual defects at or adjacent to the site of a prosthetic patch or device (which inhibit endothelialisation) [53] [48]
• rheumatic heart disease [NB7].

EBI4: Symptoms are not sufficient for diagnosis; imaging is essential for confirmation.

NB7: Endocarditis prophylaxis was previously only recommended for rheumatic heart disease in Aboriginal and Torres Strait Islander peoples, or considered for people with rheumatic heart disease at significant socioeconomic disadvantage. However, studies have demonstrated that rheumatic heart disease is an independent risk factor for the development of and adverse outcomes from infective endocarditis [1] [3] [20].

Electrical Dysrhythmias⁶⁴

• Extrasystoles (ectopics)
• Tachycardia (including Atrial fibrillation)
• Bradycardias

Aetiology and Manifestations of Dysrhythmias⁶⁵

• Definition: An alternation in the normal rhythm of the heartbeat.
• Epidemiology: 15% of the population
• Aetiology: disorders in heart automaticity (impulse formation) or conductivity (block or delay)

Abnormal impulse generation	Abnormal impulse conduction
Sinus bradycardia <60 bpm	AV Block – delay/failure conduction from atria to ventricles
Sinus tachycardia >100 bpm
Atrial flutter
Atrial fibrillation – acute/chronic
Premature ventricular contractions
Ventricular tachycardia
Ventricular fibrillation
Ventricular extrasystole

Causes⁶⁶

• Cardiac disease
• Drugs: caffeine, alcohol, smoking, β-2-agonists, digoxin, dopamine, tricyclics, tobacco
• Metabolic changes: catecholamines, autonomic/endocrine disease, hyperthyroidism, fever, hypoxia, surgery, persistent vegetative neurological states
• Electrolyte imbalance: e.g. secondary to CKD
• Respiratory: COPD

Signs/Symptoms⁶⁷

• Most frequent symptom: Palpitations.
• Others: sickness, syncope, dyspnoea, anxiety, fatigue, chest pain, dizziness.
• May have no symptoms

Classification

• Rate:
  • Tachycardia (fast rate >100 bpm)
  • Bradycardia (slow rate <60 bpm day, <50 bpm night)
  • Irregular
• Mechanism: automaticity, re-entry, fibrillation
• Origin: atrium, ventricle

Types of Arrhythmias⁶⁸

Extrasystoles

• Premature beats
• Atrial extrasystoles
• Ventricular extrasystoles

Inherited Disorders

• Long QT syndrome
• Brugada syndrome

Bradycardias

• Sinus bradycardia
• Sinus arrest
• Atrioventricular block, bundle branch block, heart block

Tachycardias

• Sinus tachycardia
• Sinus node re-entrant tachycardia
• Atrioventricular tachyarrhythmia
• Supraventricular tachycardia
  • Atrial flutter
  • Atrial fibrillation
    • Paroxysmal AF
    • Persistent AF
    • Permanent AF
  • Paroxysmal atrial tachycardia
  • Paroxysmal supraventricular tachycardia
  • Wolff-Parkinson-White syndrome - Atrial Fibrillation (AF) is the most common arrhythmia (1% of population) and carries a high risk of stroke; patients are usually anticoagulated.
• Ventricular tachycardia
• Ventricular fibrillation

General Management and Cardiac Electronic Devices⁶⁹⁷⁰

Identify cause – May only need treatment for this

If no underlying cause – Treatment depends on type/severity of arrhythmia. Focus: controlling RATE and RHYTHM

Treatments

• Medications
• Pharmacological cardioversion
• Electric cardioversion
• Pacemaking / Defibrillation
• Surgery

Cardioversion⁷¹

• Restores regular rhythm
• Pharmacological (chemical) cardioversion
• Electrical cardioversion

Cardiovascular Implantable Electronic Devices (CIEDs)

• Permanent pacemakers
• External cardiac defibrillators
• Ventricular assistive devices (VAD)
• Implantable Cardioverter Defibrillator (ICD)
• Pacemakers: Stimulate the heart when the rate is too slow.
• ICDs: Administer shocks to stop dangerous rhythms.

Radiofrequency Ablation (Catheter Ablation)

Dental Management of Dysrhythmias⁷²⁷³⁷⁴

Anti-arrhythmic Drugs⁷⁵

• Gingival swelling = verapamil/diltiazem (Ca-channel blockers), enalapril (ACE inhibitor)

• Lichenoid ulceration and oral ulceration related to agranulocytosis = some β-blockers

• Lupus-like reaction and mucosal ulcers due to agranulocytosis = procainamide

• Xerostomia = disopyramide

• Anticoagulation (see Bleeding Disorders lecture)

• Oral side effects of drugs (see Hypertension section)

• CIED interference

• Patients with CIED can undergo most general dental treatment.

• Surgical diathermy can interfere with some CIEDs (especially monopolar).

• With modern CIEDs, interference from most other dental electronic and ultrasonic devices is usually not clinically significant.

  • Interference from ultrasonic scalers or apex locators is rare with modern shielded devices.

• Consult cardiologist if in doubt.

• CIED is not an indication for surgical nor IE antibiotic prophylaxis.

Patient Safety

Be aware that an ICD shock may cause the patient to flinch or bite down suddenly during treatment.

• LVADs increase risk of thrombotic events ∴ increased risk of post-op bleeding.
  • Patients may be on antithrombotics.
  • LVAD-induced blood pressure changes.

Further info on interference (American Dental Association): https://www.ada.org/resources/ada-library/oral-health-topics/cardiac-implanted-devices-and-electronic-dental-instruments

Access⁷⁶

• Peak endogenous epinephrine levels in early morning → ideally appointments late morning or early afternoon.
• High risk patients – treated in hospital.

Education/Prevention

• Oral side effects of medication.

Surgery

• Liaise with cardiologist if concerned about CIED interference.
• Pre-operative: anxiety management, check INR if warfarinated, defibrillator readily available.
• Peri-operative:
  • Positioning: supine if pacemaker.
  • LA: adequate provision, judicious use of vasoconstrictor, avoid intravenous injection.
  • Sedation: oxygen saturation monitoring, may be helpful to minimise stress.
• Post-operative: haemostasis if anticoagulated.

Muscular Cardiomyopathies⁷⁷⁷⁸⁷⁹

Primary – genetic/inherited, acquired

Secondary

CARDIOMYOPATHIES

Definition: broad term for diseases of the heart muscle that result in reduced ability for the heart to pump blood to the rest of the body.

• Manifests as fatigue, shortness of breath, and peripheral edema.

Aetiology

Primary

Genetic/Inherited

• Hypertrophic cardiomyopathy (HCM)
• Dilated cardiomyopathy (DCM)
• Arrhythmogenic R ventricular (ARVC)

Acquired

• Alcohol, chemotherapeutics (most common acquired cause)
• Tako-tsubo cardiomyopathy
• Tachycardia induced
• Muscular dystrophies

Secondary

• Storage: haemochromatosis, Fabry disease
• Infiltrative: amyloidosis, Hurlers syndrome
• Toxicity: alcohol, radiation
• Nutrition: Beri-beri, Kwashiorkor
• Autoimmune: SLE, RA
• Neuromuscular: Friedrich’s ataxia
• Endocrine: Diabetes, thyroid disease, phaeochromocytoma

Signs/Symptoms

Management

- Oedema (pulmonary, peripheral – ankles & legs, abdominal) - Thrombi/emboli/clot formation - Exertional and paroxysmal nocturnal dyspnoea (SOB) - Arrhythmias - Nausea - Chest pain - Palpitations - Fainting - Sudden cardiac death

- Lifestyle changes: diet, exercise, stress, avoid tobacco/alcohol - Medications: hypertension drugs, anti-arrhythmic drugs, oral anticoagulants. Often: beta blockers, potassium channel blockers. Other: CCBs (verapamil, diltiazem) +/- ACEIs, diuretics, digoxin. - Devices to correct arrhythmias: pacemakers, ICDs - Devices to improve blood flow: LVAD, cardiac resynchronisation therapy (CRT) - Procedures: catheter ablation, heart transplant

Congenital Heart Disease⁸⁰

CONGENITAL

Cyanotic

Acyanotic

Definition⁸¹

• Any congenital structural defects of the heart (including valve stenosis or septal defects) or adjacent great vessels that lead to malfunction (arrhythmias or flow problems). Can be alone or in combinations.

Epidemiology

• Is the most common type of heart problem in children (1% live births). 20% also have other congenital anomalies.
• Diagnosed in at least 1 in 180 births (1-2% of the population).

Aetiology⁸²

• Often unidentified, multifactorial, genetic, and environmental factors.
• Acquired causes:
  • maternal infections (Rubella, Cytomegalovirus)
  • maternal drug use (alcohol, anticonvulsants, lithium, thalidomide, warfarin, other drugs)
  • maternal systemic disease (SLE, diabetes); maternal irradiation (rare).
• Genetic syndromes with cardiac defects:
  • Chromosomal: Downs, Edwards, Turners
  • Hereditary: Ehlers-Danlos syndrome, Marfan syndrome, osteogenesis imperfecta, mucopolysaccharidosis, Holt-Oram syndrome, Noonan syndrome, Williams syndrome

Classification⁸³

• Cyanotic (R to L shunting): shunting deoxygenated blood from the right ventricle into the left side of the heart and the systemic circulation (bypassing the lungs)
• Acyanotic (obstruction, or L to R shunting): blood contains enough oxygen but is pumped abnormally around body, forcing the heart to work harder

Cyanotic	Acyanotic, no shunt	Acyanotic with shunt
Tetralogy of Fallot	Aortic stenosis	Atrial septal defect
Eisenmenger syndrome	Bicuspid aortic valve	Patent ductus arteriosus
Pulmonary atresia	Coarctation of the aorta	Ventricular septal defect
Pulmonary valve stenosis	Dextrocardia
Total anomalous venous drainage	Mitral valve prolapse
Transposition of the great vessels
Tricuspid atresia

Complications⁸⁴

• Arrhythmias
• Infective endocarditis
• Stroke (cerebral abscess)
• Pulmonary hypertension and oedema
• Polycythaemia/bleeding tendency/thrombotic tendency
• Heart failure

Oral Manifestations⁸⁵⁸⁶

• Delayed eruption of both dentitions
• Positional anomalies
• Enamel hypoplasia
• Gross vasodilatations in the pulps
• Cleft palate
• Fissure tongue
• Greater caries and periodontal disease (associated to poor oral hygiene and lack in dental attention).
• Increased risk of periodontal disease can be attributed to “treatment burnout” in patients and caregivers.

Cardiac Failure⁸⁷⁸⁸

Definition: When structural or functional impairment of the pumping action of the heart leads to blood output insufficient to meet the body’s demands → lack of tissue and organ perfusion

Aetiology: any structural or functional cardiac or non-cardiac disorder that impairs ability of heart to respond to physiological demands for CO

Main causes of heart failure⁸⁹

Left-sided mainly	Right-sided mainly	Biventricular
Ischaemic heart disease	Chronic obstructive pulmonary disease	Ischaemic heart disease
Aortic valve disease	Pulmonary embolism	Aortic valve disease
Mitral valve disease		Mitral valve disease
Hypertension		Hypertension
		Cardiomyopathies
		Hyperthyroidism
		Chronic anaemias
		Arrhythmias

Left-sided heart failure⁹⁰

Left side of heart can’t pump blood out of heart so blood backs up into the LUNGS

• Left-sided failure primarily presents with pulmonary issues such as cough, crackles, and shortness of breath.

Right-sided heart failure

Right side of heart can’t pump received blood to the lungs so blood backs up into the BODY

• Right-sided failure primarily presents with systemic issues like peripheral edema and liver enlargement.

Symptoms

• Pulmonary congestion:
  • Cough
  • Crackles
  • Pink-tinged sputum
  • Tachypnea
• Tachycardia
• Fatigue
• Cyanosis
• Exertional dyspnea
• Peripheral edema
• Ascites
• Enlarged liver & spleen
• JVD
• Weight gain
• Increased peripheral venous pressure

Edema

Lifestyle changes	Pharmacologic	Devices	Surgical intervention
- Fluid & salt management (limit intake)

• Minimise alcohol intake

• Gentle exercise | - Inotropes e.g. digoxin (AF)

• Diuretics e.g. thiazide

• ACE inhibitors

• β blockers

• Vasodilators

• Aldosterone antagonists | - Pacemaker

• Cardiac resynchronisation device

• ICD | - Revascularisation procedures (CABG)

• Valve replacement / repair (due to valve damage: CHD, IE, MI)

• Heart transplantation (end stage) |

• Do not undertake dental treatment unless medical practitioner advised HF is stable

• Limit duration of dental procedures

• Patient may be unable to lie horizontally

  • Position dental chair with head higher than heart
    • Treat the patient in a semi-supine position to avoid respiratory distress.
  • Comfortable position for sleeping → “how many pillows do you use when sleeping?”

• Increased risk with sedation and GA → hospital environment with anaesthetist

• Avoid NSAIDs if possible

  • Especially if diuretic + (ACEI or A2RB) → risk of acute kidney injury

• Diuretics + drugs with diuretic effect (e.g. dapagliflozin, empagliflozin) → dry mouth

• May be candidate for heart transplant

  • Require dental assessment before being waitlisted
  • Optimise oral health
  • May seek hospital dental specialist for advice for pre-transplant dental treatment plan

Cardiac Surgery and Perioperative Management

Cardiac Surgery Work-Up⁹¹

Types of Cardiac Surgery⁹²

• Coronary angioplasty and stent (bare metal or drug-eluting) = Percutaneous coronary intervention (PCI)
  • Improve blood flow through occluded coronary arteries
• Coronary artery bypass grafting (CABG)
  • Redirect blood flow around occluded coronary arteries
• Valve replacement or Transcatheter aortic valve implantation (TAVI)
  • Replace faulty or damaged heart valves
• Congenital correction
  • Repair abnormal or damaged structures
• Pacemaker or Implantable Cardioverter Defibrillator (ICD) placement
  • Implant devices to control heart beat or support function / blood flow
• Cardiac Transplant
  • Replace a damaged heart, severe heart failure

Risks and Benefits of Preoperative Dental Treatment

Cardiac Risks of Dental Treatment⁹³⁹⁴

• Risk stratification guidelines: Peri-operative risks for CVD patients undergoing non-cardiac surgical procedures
• H&N surgery 1-5%, dental surgery / superficial surgery <1%
  • European Society of Cardiology (ESC) and European Society of Anaesthesiology (ESA) (Halvorsen et al., 2022)
  • American College of Cardiology (ACC) and American Heart Association (AHA) (Thompson et al, 2024)
• Smith et al 2014:
  • Prophylactic dental extractions prior to cardiac surgery carries a 3% risk of death and 8% risk of major adverse outcome before cardiac operation

Smith MM, Barbara DW, Mauermann WJ, Viozzi CF, Dearani JA, Grim KJ. Morbidity and Mortality Associated with Dental Extraction Before Cardiac Operation. Ann Thorac Surg. 2014; 97: 838-44.

”… raises the question whether we should in fact get on with our cardiac operations and deal with the dental work at some other time, if at all, or risk killing patients with good intent!”

Unsworth-White 2014 (commentary of Smith et al 2014)

Unsworth-White MJ. Invited Commentary - Morbidity and Mortality Associated with Dental Extraction Before Cardiac Operation. Ann Thorac Surg. 2014;97,844.

Management of perioperative acute pain and infection (pus, swelling, cellulitis) needs to be a joint decision between the dentist and the physicians caring for the patient planned for cardiothoracic surgery.

But when should we treat chronic, asymptomatic pathology?⁹⁵

Risks outweigh benefits

• Ischaemic disease (eg. CABG, PCI, stent, angioplasty)
• Rhythmic disease (eg. ICD/pacemaker, ablation)

Benefits may outweigh Risks

• Valvular disease (eg. replacement, repairs, TAVI)
• Infective endocarditis (often leads to valvular surgery)
• Heart transplant (heart failure)

Ischaemic Indications – Risks vs Benefits of Pre-Op Dental Treatment^96979899

Potential benefits:

• Decrease endogenous catecholamine release (resulting in increased BP) if patient is in pain
• Reduce pre-operative infection risk or graft rejection
  • Limited literature regarding dental extractions prior to CABG or heart transplant surgery
• Lack of clear evidence to support the reduced risk of post-operative infection (Meyer et al., 1999)

Risks outweigh benefits	Benefits may outweigh Risks
Ischaemic disease (eg. CABG, PCI, stent, angioplasty)

- <mark>It is generally better to defer dental treatment until after revascularization (CABG/Stent) when the heart has better oxygen supply.</mark> | Valvular disease (eg. replacement, repairs, TAVI)
- <mark>More aggressive dental treatment is often performed preoperatively to prevent postoperative infective endocarditis.</mark>

Rhythmic disease (eg. ICD/pacemaker, ablation) | Infective endocarditis (often leads to valvular surgery) | Heart transplant (heart failure)

Management of perioperative acute pain and infection (pus, swelling, cellulitis) needs to be a joint decision between the dentist and the physicians caring for the patient planned for cardiothoracic surgery.

Clin Oral Invest (1999) 3:79–83 © Springer-Verlag 1999

ORIGINAL ARTICLE

U. Meyer · D. Weingart · M.C. Deng · H.H. Scheld · U. Joos Heart transplants – assessment of dental procedures

Received: 25 September 1998 / Accepted: 26 February 1999

Abstract The object of this study was to evaluate the effects of dental foci on survival rates and rejection episodes in heart transplant recipients. Therefore, in a retrospective longitudinal study we studied 74 heart transplant recipients at the Department of Maxillofacial Surgery and Department of Thoracic and Cardiovascular Surgery, University of Münster. Study patients were divided into groups; those in which dental foci had been verified (n=31) and those without dental foci (n=43). Statistical analysis was performed using the chi-square test, Kaplan-Meier life table analysis, and the log-rank test. Before heart transplantation, patients were screened clinically and radiographically to determine the extent of dental foci. Postoperatively, patients were evaluated dentally and medically to identify the impact of dental foci on the incidence of systemic and oral infections, frequency and severity of rejection episodes, mortality, and complications arising during dental treatment. By comparing the mortality, infection and rejection rates in the various groups no statistically significant differences (P>0.05) were found between patients. Despite immunosuppression, extended inflammatory processes such as abscess formation or viral stomatitis were not found in the oral cavity. We therefore suggest that patients suffering from the symptoms of severe heart failure need not be subjected to rigorous preoperative dental treatment.

Key words Heart transplant · Dental treatment · Mortality

Introduction The survival rate of patients after heart transplantation has improved due to recent advances in perioperative management and immunosuppression [7]. Preoperative evaluation includes assessment of dental foci and their subsequent eradication [13, 3, 5]. So far, no study has examined the need for such a radical approach. Most microorganisms associated with bacteriemia in patients with heart transplantation are commensal organisms of the oral cavity [5]. Systemic infections and rejection dramatically decrease the survival rate in patients subjected to heart transplantation. Since odontogenic inflammation may favor transplant rejection [5], cause bacterial endocarditis and may lead to life-threatening postoperative infections [2], all existing or potential sources of dental infection should be eliminated before heart transplantation. To our knowledge, specific guidelines specifying the extent of such dental procedures do not exist. The purpose of this study was to analyze the complication rates in patients in whom dental foci had been verified as compared with patients without dental foci so that the role of these foci on the postoperative outcome of heart transplantation could be determined. The influence of various dental foci on differences in survival and rejection probabilities of heart transplant recipients was investigated to reevaluate our dental treatment protocols.

Clinical Decision Making and Future Proofing

To Proceed or Not to Proceed?¹⁰⁰

• Recommendation: integrated team decision based on individual situation of the patient (stable vs unstable condition)
• Dental treatment need
• Severity of cardiac disease (e.g. chest pain at rest, triggers/frequency, number of medications)
• Type and magnitude of dental procedure
  • Weigh the “treatment burden” against the severity of cardiac disease.
• Stability and cardiopulmonary reserve (functional capacity)

How Far Ahead to Future Proof?¹⁰¹

“IN THE 12 MONTHS AFTER MYOCARDIAL INFARCTION, STENT PLACEMENT, CORONARY ARTERY BYPASS SURGERY, OR VALVE PROCEDURES (INCLUDING TRANSCATHETER AORTIC VALVE IMPLANTATION [TAVI]), PATIENTS ARE AT INCREASED RISK OF A MAJOR ADVERSE CARDIAC EVENT (e.g. SUDDEN DEATH).

DEFER ELECTIVE DENTAL TREATMENT FOR 6 MONTHS AFTER MYOCARDIAL INFARCTION, STENT PLACEMENT, CORONARY ARTERY BYPASS SURGERY OR VALVE PROCEDURE.

IF DENTAL PAIN OR INFECTION OCCURS WITHIN 6 MONTHS FOLLOWING THE EVENT, PROVIDE ADEQUATE EMERGENCY TREATMENT BUT AVOID THE USE OF ADRENALINE-CONTAINING LOCAL ANAESTHETICS. CONSIDER SEEKING SPECIALIST ADVISE ABOUT APPROPRIATE TREATMENT AND TIMING OF PROCEDURES.”

Oral & Dental Therapeutic Guidelines v4 2026

Thinking It Through… Cardiac Surgery¹⁰²

Rationale

• Does need for dental treatment outweigh the cardiac risks?
• Direct effect on cardiac outcome = Endocarditis risk

Medical, Dental and Social Considerations

• Bacteraemia risk of dental pathology
• Amount of treatment patient can tolerate in one go vs risks of performing over multiple visits
• Anticoagulation / antiplatelet drugs (prophylactic vs therapeutic)
• Antibiotic prophylaxis
• Focus on preventive oral hygiene to reduce daily bacteraemia

Entire or Localised Areas of the Mouth

• Entire dentition

Optimal Timeframes

• Urgency for cardiac surgery
• Future-proof for next 6 months (i.e. optimise for the short-term)
  • Aim to make the patient dentally stable for at least 6 months post-surgery, as elective care is deferred during this high-risk recovery period.

Treatment Approaches

• Aggressive (e.g. typically insufficient time to assess periapical response to RCT)
  • Treatment is often more aggressive (extractions over RCT) because there is no time to monitor healing before urgent surgery.

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Clinical Cases

Case: Gingival Hyperplasia from Calcium Channel Blockers

Question

The lecturer presents a scenario involving patients taking calcium channel blockers (specifically dihydropyridines). What are the characteristic oral findings associated with this medication, and what factors exacerbate the condition?

Findings and Reasoning

• Observation: The lecturer describes “really swollen gums” or gingival hyperplasia.
• Mechanism: This is a known side effect of dihydropyridine calcium channel blockers (and sometimes ACE inhibitors).
• Exacerbating Factors: The presence of poor oral hygiene and plaque can significantly worsen the extent of the gingival enlargement.
• Management: If the enlargement is extensive, it may require specialist periodontal and medical management.

Case: Oral Ulceration from Nicarandil

Question

What specific oral manifestation is “classically known” to be associated with the drug Nicarandil, often used for ischemic heart disease?

Findings and Reasoning

• Observation: Nicarandil is associated with oral ulceration.
• Other Potential Signs: It can also lead to facial flushing and lupoid lesions.
• Clinical Significance: When a patient with ischemic heart disease presents with oral ulcers, the clinician should consider Nicarandil as a potential contributing cause.

Case: Angina Radiating to the Jaw

Question

How might a cardiac event be mistaken for a dental problem, and what is the key clinical “clue” to differentiate them?

Findings and Reasoning

• Scenario: Angina pain can radiate to the lower jaw and the teeth.
• Differential Diagnosis: This can be mistakenly identified as being of dental origin.
• Key Diagnostic Clue: If the onset of the pain is associated with physical exertion, it is much more likely to be angina rather than a primary dental or maxillofacial problem.

Case: Oral Manifestations of Congenital Heart Disease

Question

In children with congenital heart disease, what specific dental and oral anomalies might be observed during a clinical examination?

Findings and Reasoning

• Developmental Findings:
  • Delayed eruption of both primary and permanent dentitions.
  • Positional anomalies of the teeth.
  • Enamel hypoplasia.
• Structural Findings:
  • Grossly enlarged (dilated) pulp chambers.
  • Association with cleft palate or fissured tongue.
• Reasoning: These anomalies occur because congenital heart disease affects the overall growth and development of the child.

Case: Left-Sided vs. Right-Sided Heart Failure

Question

The lecturer contrasts the clinical presentations of left-sided and right-sided heart failure. What are the observable signs for each?

Findings and Reasoning

• Left-Sided Heart Failure (Pulmonary focus):
  • Cough and crackles in the lungs.
  • Pink-tinged sputum.
  • Tachycardia and cyanosis.
• Right-Sided Heart Failure (Systemic focus):
  • Peripheral edema (swelling in the limbs).
  • Liver issues and splenomegaly (enlarged spleen).
  • Weight gain.
• Clinical Application: For patients with heart failure, the lecturer notes they may not tolerate a horizontal position. A clinical tip is to ask the patient how many pillows they use to sleep and recline the dental chair only to that comfortable level.

Footnotes

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