16. 2024 Lecture 16 DentistryCardiovascular2

Cardiovascular Disease

  • Major cause of morbidity and mortality.

  • Focus areas: hypertension, angina pectoris, myocardial infarction (MI), arrhythmias, and heart failure.

Angina Pectoris

  • Chest pain due to mismach of oxygen demand and supply in cardiac m . worse during physical exertion or emotional anxiety - activation of sympathetic nervous system, increase noradrenaline release, increase cardiac work

  • Chest pain that may radiate to the arm, neck, or jaw due to ischemic heart disease from coronary atherosclerosis.

  • Stable angina resolves with rest; persistent pain at rest suggests unstable angina or imminent MI.

Rationale for Drug Use in Angina

  • Increase coronary blood flow to enhance oxygen supply to heart muscle.

  • Reduce cardiac work to decrease oxygen demand by the heart muscle.

  • Decrease clotting in diseased arteries using anti-platelet agents (anticoagulants).

Drugs Used to Treat Angina Pectoris

  • Organic Nitrates: e.g., glyceryl trinitrate (GTN), isosorbide dinitrate (ISDN), isosorbide mononitrate (ISMN).

  • Beta Blockers: Reduce heart rate and myocardial oxygen demand.

  • Calcium Channel Modulators: e.g., rate-limiting agents (verapamil, diltiazem).

  • Others: Nicorandil, ivabradine,

  • anti-platelet drugs, and anticoagulants.

Organic Nitrates

Specifics

  • GTN: Poor oral bioavailability, sublingual tablet, aerosol spray

  • ISDN: Longer-acting, better oral bioavailability.

  • ISMN: transdermal patch, Longer-acting, better oral bioavailability.

Mechanism of Action

  • Drugs are metabolised to nitric oxide (NO) by enzyme in the smooth muscle via a sulfhydryl dependent mechanism (tissue -SH group)

  • NO activates guanylate cyclase in the cytosol, produce cGMP, which is a second messenger.

  • cGMP activates protein kinase G, leading to the phosphorylation and inactivation of myosin light chain kinase.

  • hyperpolarization, decrease calcium entry into muscle cells

  • leading to relaxation of vascular smooth muscle and vasodilation.

  • Dilate systemic veins more than arteries, reducing preload and cardiac work, decreasing oxygen demand.

  • dilate coronary arteries → inprove oxygen delivery to cardiac muscle Improve blood flow to ischemic areas by dilating obstructed epicardial arteries or collateral vessels.

  • Redistribute blood in the heart from epicardial to endocardial areas vulnerable to ischemia.

Adverse Effects

  • Postural hypotension, flushing, headaches, xerostomia, possible tachycardia.

Adverse Effect - Nitrate Tolerance

  • Loss of drug effect with continued usage, especially through patches; allow 8-12 hours nitrate-free periods daily

  • cause depletion of tissue SH groups

  • May be reversed by sulfhydryl (SH) donors, e.g., N-acetylcysteine.

Management of Angina

  • For acute relief, administer sublingual GTN

  • To prevent angina attacks, use beta blockers or calcium channel modulators, often in combination with nitrates.

  • Long-term management may also include isosorbide mononitrate.

Beta Blockers

not done

  • effective in prophylaxis of stable angina.

  • directly - Decrease myocardial oxygen demand by reducing heart rate and contractility

  • indirectly -reduce peripheral vasclear resistance

  • Caution: May worsen vasospasm in variant angina.

Calcium Channel Modulators

  • All lower blood pressure, reducing cardiac afterload and indirectly decreasing oxygen demand.

  • Dilate epicardial coronary arteries and improve blood flow supply to ischemic areas.

  • Rate-limiting calcium channel blockers have negative inotropic effects, further reducing cardiac work.

Nicorandil

  • Acts as both a potassium channel opener and a nitrate; relaxes vascular smooth muscle.

  • Side effects include flushing, dizziness, and headache, oral ulceration

Ivabradine

  • Reduces heart rate by inhibiting If channels; an alternative/additive to beta blockers.

  • Side effects: bradycardia, heart block, and enhanced brightness, blurred vision.

Acute Coronary Syndrome

  • Encompasses ST-Elevation Myocardial Infarction (STEMI), Non-ST Elevation Myocardial Infarction (NSTEMI), and unstable angina.

  • Troponin markers for cardiac damage used to diagnose.

Management Post-MI

  • Provide supportive care, manage pain with GTN, offer oxygen, and possibly morphine.

  • Use aspirin to prevent cardiac injury and restore coronary blood flow rapidly through reperfusion therapy.

  • Dual antiplatelet therapy (DAPT) in hospital care alongside anticoagulants.

Long-term Management Post-MI

  • Beta Blockers: To lower myocardial oxygen consumption and reduce further infarction risk.

  • ACE Inhibitors (or ARB): To prevent left ventricular dysfunction and heart failure progression.

  • Low-dose Aspirin: For ongoing prevention.

  • Nitrates

  • Consider lifestyle changes and cardiac rehabilitation for comprehensive recovery.

Arrhythmias

Supraventricular Tachycardias

  • Abnormal fast heartbeat due to increased automaticity or re-entry of impulses; includes atrial fibrillation.

  • Symptoms: palpitations, fainting, sweating, and breathlessness.

Management of Atrial Fibrillation

  • Focus on rate and rhythm control, using beta blockers, calcium channel modulators, electrical cardioversion, and anticoagulants for stroke prophylaxis.

Chronic Heart Failure

Definition and Causes

  • Heart cannot supply sufficient blood to meet metabolic needs; causes include myocardial infarction and chronic coronary atherosclerosis.

Symptoms

  • Reduced exercise tolerance, breathlessness, and signs of fluid overload (e.g., edema).

Consequences

  • Compensatory mechanisms (SNS and RAAS) lead to further deterioration; significant morbidity and mortality risks.

Drugs for Heart Failure

  • Diuretics: Mainly loop diuretics like furosemide for symptom relief; do not improve survival.

  • ACE Inhibitors and ARBs: Suppress RAAS activity, prolong survival, and manage symptoms.

  • Beta Blockers: Helpful in stable chronic heart failure; reduce heart rate and improve filling.

  • SGLT2 Inhibitors: Benefits beyond glycemic control; improving prognosis in heart failure patients.

Management of Acute/Decompensated Chronic Heart Failure

  • Use i.v. diuretics and vasodilators, monitor beta blocker dosing closely due to arrhythmia risks.

Application in Dentistry

  • Handle patients with histories of angina or heart failure carefully; ensure emergency medications (e.g., GTN) are available, and know management protocols for acute episodes.

  • •stop dental work

    •sit the patient upright with legs down

    •administer oxygen if possible

    •2 puffs of sublingual GTN may be useful

    •Entonox (or small dose of morphine if available) may be helpful if shortness of breath continues and patient is anxious

    •ambulance (depending on setting)

    •

Learning Outcomes

  • Identify drugs for angina, MI management, atrial fibrillation, and chronic heart failure; understand their mechanisms, uses, and adverse effects.

  • Discuss management strategies for patients with acute symptoms during dental procedures.