Coronary Heart Disease pt.2

Pathological Refresher Overview

This section provides a foundation for understanding heart failure and its mechanisms, particularly in relation to myocardial infarction and its consequences on cardiac function.

ST Segment Elevation and Myocardial Infarction

  • ST Segment Elevation: An elevation in the ST segment of an ECG is indicative of ischemia and is often associated with significant blockage, especially in coronary arteries such as the left anterior descending coronary artery. This blockage leads to reduced blood flow and oxygen to the heart muscle, potentially resulting in myocardial infarction (AMI).

  • ECG Changes: The changes observed in an ECG are due to the occlusion of the vessel, which leads to damaged heart tissue. Survivors of severe ischemic events may experience chronic conditions like heart failure.

Types of Heart Failure

  • Chronic Heart Failure: The discussion emphasizes various forms of heart failure, particularly in elderly patients, resulting in symptoms such as:

    • Swelling (Odeama)

    • Shortness of Breath (Dyspnea): Notable when lying flat (orthopnea).

  • Clinical Case Example: An elderly male patient presents with:

    • Symptoms: Shortness of breath, enlarged liver, dilated ankles.

    • Ejection Fraction (EF): A significantly low EF of approximately 20%, indicating severe impairment in the heart's pump function.

  • Dilated Cardiomyopathy: This type of heart failure may be secondary to a viral infection, illustrating that heart failure can arise from different underlying causes, including ischemic damage from AMI or other conditions unrelated to the coronary arteries.

Signs and Symptoms of Heart Failure

  • Symptoms Include:

    • Dyspnea: Often accompanied by orthopnea.

    • Oedema: Can occur in pulmonary (left side failure) or systemic (right side failure) circulation.

    • Tachycardia: The heart compensates for reduced cardiac output (CO), which fails to meet metabolic demands.

  • Biventricular Dysfunction: Heart failure often affects both sides, leading to overall cardiac dysfunction.

Causes of Heart Failure

  • Common Causes:

    • Coronary Heart Disease (CHD) and Atherosclerosis as primary contributors.

    • Potential comorbidities including hypertension and pulmonary hypertension.

    • Also includes cardiomyopathy, valve complications, and issues with electrical conduction.

Heart Failure Classifications

  • Systolic vs. Diastolic Dysfunction:

    • Systolic Dysfunction (HFrEF): Characterized by impaired contraction leading to reduced ejection fraction. Typically associated with ischemic heart disease and can follow AMI or other muscle dysfunction.

    • Diastolic Dysfunction (HFpEF): The heart can contract but cannot fill properly under stress. Characterized by normal EF at rest.

  • Trends: HFpEF is increasing, particularly in the elderly, often associated with fibrosis and more prevalent in females, especially diabetic women.

Cardiac Remodeling

  • Ventricular Changes:

    • Diagrams illustrating remodeling in chronic heart failure and post-AMI. HF with reduced EF is characterized by dilation of the heart and lower ejection fractions.

  • Normal EF Ranges: Normal ejection fraction is typically between 60%-70%.

Compensatory Mechanisms

  • Baroreceptor Reflex: If there’s a decrease in CO, several compensatory mechanisms will activate:

    • Increased Sympathetic Drive: Enhanced force and rate of contraction via norepinephrine adjustment and peripheral vasoconstriction.

    • Renal Compensations: Includes renin release that leads to angiotensin II formation, which is responsible for vasoconstriction and signaling aldosterone release for sodium retention.

  • Downstream Effects: Compensatory responses, while immediate aids, can lead to worsening heart failure due to increased afterload and myocardial oxygen demand.

Treatment Approaches

  • Lifestyle Modifications: Importance of diet, weight control, and gradual exercise as foundational strategies in managing heart failure.

  • Pharmacological Strategies: Focus on two main treatment mechanisms:

    • Angiotensin Mechanisms:

    • ACE Inhibitors: Block the formation of angiotensin II, reduce vasoconstriction, decrease blood pressure, and cause sodium and water excretion. Examples include captopril, enalapril and perindopril.

    • Angiotensin II Receptor Blockers (ARBs): Prevent angiotensin II from binding to its receptors, blocking its effects. Common ARBs include losartan, irbesartan, and candesartan.

    • Adverse Effects:,

    • ACE inhibitors: Cough (due to bradykinin accumulation), hypotension, hyperkalemia, and other potential effects such as rash or angioedema. Special care is needed in pregnancy.

    • ARBs: Similar profile but generally better tolerated regarding cough since they do not impact bradykinin levels.

Angiotensin System Overview

  • Renin-Angiotensin-Aldosterone System (RAAS):

    • Angiotensinogen produced in the liver, is cleaved by renin into angiotensin I, which is converted to angiotensin II by ACE.

    • Physiological Effects of Angiotensin II: Significant vasoconstrictor, stimulates aldosterone to increase sodium and fluid retention, modifies cardiac muscle structure, and plays a role in inflammatory processes.

Clinical Implications

  • The management of heart failure remains focused on enabling heart function recovery through effective reduction in the workload and enhancement of contractility, especially in cases of reduced ejection fraction (HFrEF).

  • The role of ongoing research into fibrosis treatment and drug discovery for heart failure continues, as current medications are not optimally effective against fibrotic processes that exacerbate HFpEF.