Categories of Cardiovascular Diseases

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Cardiovascular diseases (CVD) are conditions that affect the structures or functions of your heart. It is the leading cause of mortality in India. According to global Burden of Disease study age standarized estimates, nearly a quarter of all the death in India are attributed to CVD. The age standarized CVD death rate of 272 per 1,00,000 population in India is higher than global average of 235 per 1,00,000 population. 

CVD affects patients in many aspects of performance areas (activities of daily living, work, lesiure), performance components (muscles strength, endurance, psychological stress, cognitive disturbance), performance context (social participation, disability status, development).

In this article we will focus on various  categories of Cardiovascular Diseases. In previous blog we had discussed about Basics of Cardiovascular System : Structure and Function. (Click in on the below link to open the blog)

https://otpthealthcarerehab.blogspot.com/2020/08/basics-about-cardiovascular-system.html

Cardiovascular Disease can be divided into following categories :

1. Coronary Artery Disease : Myocardial infarction, Stable angina and unstable angina
2. Valvular Heart Disease : Acute Rheumatic disease, Infective endocarditis, Marfan's syndrome, Mitral stenosis, Mitral regurgitation or mitral valve prolapse, Aortic stenosis, Aortic regurgitation
3. Cardiac Arrhythmias : Atrial flutter, Atrial fibrillation, Ventricular fibrillation, Ventricular tachycardia, Narrow QRS Tachycardia, Heart block or Conduction block, Cardiac arrest and sudden death
4. Cardiomyopathy : Dilated Cardiomyopathy, Hypertrophic Cardiomyopathy, Restrictive Cardiomyopathy
5. Heart failure (due to longterm occupational working, by the patient,  with the affected cardiac condition leads to compensatory structural and functional changes within heart) : cardiomyopathies, ischemic heart disease, atrial fibrillation, mitral or aortic stenosis, HTN.
6. Congenital Heart Disease : Atrial septal defect, Ventricular septal defect, Patent Ductus arteriosus, Teratology of Fallot, Coarctation of Aorta
7. Pericardium and Aorta disease : Acute Pericarditis, Pericardial Effusion, Constrictive Pericarditis, Dissection of Aorta, Thoracic aortic aneurysm

We will understand each categories in brief :

1) Coronary artery diseases (CAD) : CAD develops as a consequence of decreased blood flow to the myocardium due to coronary atherosclerosis. It begins as fatty streaks in the coronaries and other arterial beds early in life. Clinical manifestations of plaque rupture with subtotal or total occlusion of the affected artery, now called acute coronary syndrome, include acute myocardial infarction, unstable angina, and sudden death due to ventricular fibrillation. Other manifestations of CAD include stable angina, which occurs when plaque growth leads to subtotal occlusion of the artery, and ischemic cardiomyopathy. 

• Angina can be classified as stable angina, unstable angina and variant angina (Prinzmetal angina). The term stable angina refers to the predictable occurrence of pressure or choking sensation in the chest on efforts. Severity of angina can be classified using Canadian Cardiovascular Society classification.
• Stable angina : Angina occurs after strenuous or prolonged exertion. Patients experience sensations in chest of squeezing, heaviness, pressure, weight, extreme aching or burning and tightness in chest. Radiation to shoulder, neck, jaw, inner arm, epigastrium (can occur without chest component); band-like discomfort. pain lasts for 3 to 15 minutes. In ECG reading, ST  depression with or without T inversion especially if seen during an episode of angina is a strong evidence of ischemia. Sensations abates when stressor is gone or nitroglycerin is taken.
• Unstable angina : Angina of recent onset (some weeks) brought on by minimal exertion or occuring at rest or during sleep.  The main pathology is plaque rupture. There is marked limitation of ordinary activity or inability to carry out any physical activity without chest discomfort or angina at rest. Post MI angina which occur 24 hours to 2 wk after MI. ECG may show acute ST elevation or depression or no permanent change. Pain often resistant to nitroglycerine.  Angina prolonged for more than 15 minutes.
• Prinzmetal or variant angina : Vasospasm of coronaries can occur with or without atheroma of coronaries. Chest pain often occurs at rest. ECG may show transient ST elevation. It may be associated with cardiac arrhythmias such as ventricular fibrillation or tachycardia. 
• Myocardial Infarction (MI) : Irreversible necrosis of myocardial tissue on account of prolonged ischemia. Caused due to blocking of atheromatous coronary vessel supplying the cardiac muscles. Appearance of cardiac enzymes troponin in circulation, indicates MI. According to new WHO guidelines a cardiac troponin rise accompanied by either typical symptoms or pathological Q waves and ST changes (NSTEMI or STEMI) are diagnostic of MI. Myocardial ischemia is essentially due to development of atherosclerotic plaques in side the coronaries which gradually narrow the lumen. Plaque ruptures leads to platelet activation, aggregation and coagulation pathway activation and endothelial vascular constriction culminating in coronary thrombosis and occlusion. The symptoms includes : 1)The pain is severe and prolonged, lasting more than 20 minutes to several hours. 2)This pain is compressing in quality. 3)The pain is retrosternal in location. 4)The pain may radiate down the ulnar aspect of the left arm, fingers. The pain may also radiate to the neck, jaw, interscapular region. 5)The pain may be associated with severe sweating, extreme weakness or syncope or palpitations or nausea or vomiting.

Fig : CAD : Narrowing of arterial lumen due to plaque formation, plaque rupture, thrombus formation and occulsion.

Fig : Difference between Stable, Unstable, and MI.

2) Valvular Heart Disease :  it is characterized by damage to or a defect in one of the four heart valve : the mitral, aortic, tricuspid or pulmonary valve. These conditions can lead to either stenosis or regurgitation, thus affecting the normal blood flow, ejection fraction and cardiac output. It leads to retrograde increase in chamber pressure and pulmonary venous or arterial pressure. If these conditions are not treated then it will cause irreversible chamber dilatation or hypertrophy due to increased retrograde pressure and work of heart. Considering the normal blood circulation (one direction) flow, dilatation or hypertrophy occurs in preceding heart chamber to affected valve.

Fig : Valvular heart disease with either Stenosis or Regurgitation defect

Mitral stenosis : it is a condition of pathological narrowing of mitral valve. Normal square area of mitral valve is 4-6 square cm. When it is reduced to half of it, significant hemodynamic changes take place. Commonest cause is Rheumatic heart disease and rare causes are congenital, Infective endocarditis with large vegetations causing obstruction, Endomyocardial fibrosis etc. Pathology :1)Commissural fusion is the hall mark, 2)Thickening of leaflets and fibrosis, 3)Stenosis develops after a latest period of about 10 years.

Fig : Hemodynamics and pathophysiology of Mitral Stenosis 

Mitral Regurgitation : Abnormal reversal of blood flow from left ventricle to left atrium. “A defect anywhere in the mitral valve apparatus can cause Mitral regurgitation.”  Etiology of “Acute” mitral regurgitation: Infective endocarditis (perforation of leaflet), Acute myocardial infarction (rupture of chordae or papillary muscles dysfunction), acute failure of prosthetic valve, Marfan's syndrome. In rheumatic heart disease, the Cusps get retracted due to fibrosis causing failure of coaptation of cusps in systole.

Fig : Hemodynamics and pathophysiology of mitral regurgitation

Aortic Stenosis : In aortic stenosis, there is obstruction to outflow of blood from left ventricle to the aorta. This obstruction may be at the valve, above the valve-supra-valvar or below the valve-sub-valvar. Aortic stenosis is a condition where aortic valve is narrower than normal size. The normal aortic valve area averages 2.5 cm square; (range 3-4 cm square). Etiology of valvular aortic stenosis includes: Congenital, Rheumatic, calcific (degenerative), Rarely (homozygous hyperlipidemia; rheumatoid; ochronosis).

Fig : Hemodynamics and pathophysiology of Aortic Stenosis

Aortic Regurgitation : Retrograde flow from aorta into left ventricle during diastole, through incompetent aortic valve. Primary disease of aortic valve or disease of aortic root; causing stretching and dilatation of valve ring. Causes includes : Infective endocarditis, Trauma, Dissecting aneurysm of aorta, Acute rheumatic fever.

Fig : Hemodynamics and pathophysiology of aortic regurgitation.

3) Cardiac Arrhythmias : Any cardiac rhythm that deviates from the normal sinus rhythm. Caused due to a disturbance in impulse formation or conduction or both. 

Arrhythmias  due to disturbance in impulse formation includes :

1. Abnormal automaticity : the sinus node contains pacemaker cells that have spontaneous firing capacity. Abnormal automaticity occurs when other cells starts firing spontaneously, resulting in premature heartbeat.   Caused by ischemia, hypokalemia, fiber stretch, local catecholamine release.
2. Triggered automaticity : during triggered activity heart cells contract twice, although they have been activated once. Caused by after depolarization (Early or late ‘after depolarization’).  Early depolarization  often drug-induced sotalol, procainamide, quinidine. Late depolarization by digitalis.

Arrhythmias classified according to their site of origin : SA node (Sinus arrhythmia), Atria (Atrial arrhythmia), Atrioventricular junction (Junctional arrhythmia) and Ventricles (Ventricular arrhythmia).

Arrhythmias due to disturbance in impulse conduction (by re-entry) includes : Abnormal delay or block may occur anywhere along the conduction system. Classified according to site of defect: 1)SA node blocks e.g SA blocks, 2)AV blocks, e.g. I, II, III degree AV block, 3)Intraventricular blocks; bundle branch blocks.

• FIRST DEGREE HEART BLOCK : this is manifested in ECG as prolonged PR interval. The interval is more than 0.20 seconds.
• SECOND DEGREE HEART BLOCK : This can be of two types: 1) Mobitz type 1 block: It is characterized by progressive lengthening of PR interval and this is followed by a dropped beat. The block is usually in the AV node. 2) Mobitz type 2 block: In this there is block without any change in the preceding PR interval. The level of block is in the His Purkinje system.
• THIRD DEGREE COMPLETE AV BLOCK : In complete AV block, no P waves are conducted down to the ventricles. Hence the rhythm is dependent on the escape rhythm, from the bundle or ventricle. The ventricular rate is around 40 to 50 per minute. ECG is diagnostic of complete AV block.

Table : Cardiac Arrhythmias due to disturbance in impulse formation 

Fig : Cardiac Arrhythmias of atrial and ventricular origin.

The refractory period of cardiac muscles allows complete emptying of the ventricles prior to next contraction. Refractoriness of each phase of action potential is governed by the number of sodium channels ready to activate. The effective refractory period (ERP) is the amount of time in which the cell cannot respond to a new conducted stimulus. This period is how the heart stays in rhythm and prevent arrhythmias. The atrial ERP is much shorter than ventricular ERP. Problems with the atrial ERP will lead to atrial arrhythmias, such as atrial flutter and atrial fibrillation. If ERP of ventricles is affected then it leads to ventricular fibrillation. The ERP is shortened due to tachycardia and low potassium levels in body.

4) Cardiomyopathy : These are a group of diseases of the heart muscle associated with cardiac dysfunction. It is not secondary to hypertension or valvular, coronary or pericardial diseases. 

• Dilated Cardiomyopathy (DCM) consists of an enlarged left ventricular cavity with depressed systolic function. In clinical practice, patients may present in the early stage of the disease with only left ventricular dilatation, followed later by left atrial dilatation, and finally with dilatation of all four cardiac chambers.

• Hypertrophic cardiomyopathy (HCM) is characterized by a small-to-normal size left ventricular cavity, massive hypertrophy of the myocardium, and hyperdynamic systolic function. There is left ventricular hypertrophy, often with preferential hypertrophy of the interventricular septum—Asymmetrical septal hypertrophy (ASH). In addition there is mid systolic apposition of the anterior mitral wall leaflet against the hypertrophic septum—Systolic anterior motion (SAM). In majority of the patients, the left ventricular hypertrophy results in increased stiffness of the ventricle, increased diastolic filling pressure, leading into diastolic dysfunction.
• The major abnormality in Restrictive Cardiomyopathy (RCM) is diastolic dysfunction of the myocardium. Affecting either or both ventricles, RCM may cause symptoms or signs of right or left ventricular failure. Often, right-sided findings predominate, with elevated jugular venous pressure, peripheral edema, and ascites. Etiology: 1)Idiopathic, 2)Eosoniphilic endomyocardial disease, 3)Endomyocardial fibrosis (EMF), 4)Infilterative cardiomyopathies: Amyloid, hemochromatosis, 5)Scleroderma.

Fig : 3 main types of Cardiomyopathy

5) Heart Failure : Heart failure has been defined as the pathophysiologic state in which an abnormality of cardiac function or structure prevents the heart from pumping blood at a rate equivalent with metabolic requirements, or allows it to do so only when ventricular filling pressures are excessively increased.  The term Congestive heart failure refers to the complex clinical syndrome. Myocardial heart failure denotes abnormal systolic and/or diastolic function, which may be asymptomatic or progress to heart failure. The incidence of heart failure increases with advancing age.

Causes of Heart Failure :

1. Myocardial dysfunction : hypertension, ischemic heart disease, cardiomyopathy etc.
2. Obstruction to flow : Mitral Stenosis, Aortic stenosis, etc.
3. Regurgitant lesions : Mitral regurgitation, Aortic regurgitation, etc.
4. High Output states : Anemia, thyrotoxicosis
5. Restrictive ventricular filling : Constrictive pericarditis, cardiac tamponade, restrictive cardiomyopathy, etc.
6. Arrhythmias : Atrial fibrillation, Ventricular fibrillation. 

Fig : American Heart Association Stages of Heart Failure.

Table : NYHA classification for  Congestive heart failure.

Chart : Hemodynamic and pathophysiology of Heart Failure

6) Congenital Heart Disease (CHD) : A heart defect present from birth but can manifest at any time in life. The overall incidence is 8 per 1000 live births. 

Pathogenetic Mechanisms:

Pathogenesis during cardiac development varies between the different types of CHD. Hence a particular teratogen will not increase the risk of all defects. Between 5 to 8 weeks of gestation, the primitive heart tube undergoes folding, remodeling and septation that transforms its single lumen into a four-chambered heart. By the 9th week, the outflow is divided into two. For a teratogen to act on the embryonic heart to produce CHD, it has to do so during the 14 to 60 days of gestation, which is the most vulnerable period

Types of Congenital Heart Disease : 

1) Left to right shunts: atrial septal defect, Ventricular septal defect, Patent Ductus Arteriosus.

2) Obstructive lesions: Aortic stenosis, Pulmonary stenosis, Coarctation of Aorta

3) Cyanotic lesions: Tetralogy of Fallot, Transposition of great arteries

Difference between Cyanotic and Acyanotic Heart Disease

• Cyanotic heart diseases are defects that leads to mixing of oxygen-rich blood (arterial) with oxygen-poor (venous) blood. In Cyanotic heart defects, less amount of oxygen-rich blood reaches the tissues of the body for utilisation. This results in the development of a bluish coloration (cyanosis) of the skin, lips and nail beds.
• Congenital heart defects that don't normally interfere with the amount of oxygen or blood that reaches the tissues of the body are called Acyanotic heart defects. Bluish discoloration of the skin isn't common in babies with acyanotic heart defects, although it may occur during activities when baby needs more oxygen supply for tissues, such as when crying and feeding.

Fig : Classification of Cyanotic and Acyanotic Heart Disease

Diagram : Different types of commonly occurring Congenital Heart Disease 

7) Pericardium and Aorta disease : 

Pericardium diseases:

Pericardium is a bag of thin fibrous tissue. The pericardial fluid within this provides lubrication. It envelops heart and also the proximal portions of the great arteries and the veins. The visceral pericardium (single layer of mesothelial cells) is intimately attached to the epicardium. Parietal pericardium is separated from visceral by a potential pericardial space, which is filled by serous fluid and this can be up to 50 ml.  The pericardium plays an important role in preventing rapid cardiac dilatation when ventricular diastolic pressure rises acutely, but does not influence the systolic function of the heart.

• Acute Pericarditis : Acute inflammation of pericardium usually accompanied by a pericardial friction rub, chest pain and serial ECG abnormalities. Inflammation of pericardium produces fibrinous exudates which coates the pericardium and this restricts the diastolic filling.
• Pericardial Effusion : Accumulation of pericardial fluid more than the normal amount of 15-50 ml. Fluid accumulates within the closed pericardial sac. Initially the pericardium stretches but a point is reached when it cannot. At this point the heart starts getting compressed, the end point being cardiac tamponade. The effusion does not affect the systolic function; affects only diastolic filling.
• Cardiac Tamponade : Compression of heart by fluid in the pericardium, which may be blood or inflammatory exudates. Blood accumulation occurs due to trauma or ruptured pericardium. Exudate accumulation occurs  due to any pericarditis. Usually this is an acute situation requiring prompt diagnosis and urgent pericardial aspiration.
• Constrictive pericarditis (Pick's disease) is: A rigid pericardial sac caused by gross fibrosis, which limits ventricular diastolic filling. Constrictive pericarditis is the result of scarring and consequent loss of elasticity of the pericardial sac.

Fig : Pericardium disease and affect on heart chambers.

Aortic Diseases :

Aortic aneurysm is a abnormal localized dilatation of the aortic wall with its diameter 1.5 times the diameter of normal aorta. This may occur in the upper part of the aorta in the chest, known as a thoracic aortic aneurysm, or in the lower part of the aorta in the abdomen, known as an abdominal aortic aneurysm. 

• Since they represent a weakened area of the aortic wall, they are susceptible to expansion, tearing or dissection within the wall and ultimately rupture, which may cause significant bleeding and death. Early detection, surveillance and  management are critical in preventing such complications of this life-threatening condition.
• Risk factor of cause includes smoking, older age, high BP, atherosclerosis, genetic Conditions (Marfan syndrome and Ehlers-Danlos syndrome, where there is a defect in the structural support of the aortic wall, resulting in an increased risk of developing an aneurysm), Syphilis. Trauma etc.
• Signs and symptoms : Thoracic aortic aneurysms may expand slowly over time without causing any symptoms. If they become large enough, they may occasionally cause pain in the chest or back, and may exert pressure on nearby structures of the upper airway, causing cough, hoarseness of voice or shortness of breath. If the aneurysm ruptures or causes a dissection within the aortic wall, individuals typically experience a sudden onset of severe, tearing chest pain, which may spread to the neck, jaw or back. Individuals may also experience sudden difficulty breathing, loss of consciousness and signs of stroke, such as weakness and paralysis on one side of the body.

Fig : Thoracic Aortic Aneurysm

Dissection of Aorta : Aortic dissection is a serious condition in which there is a tear in the wall of the major artery carrying blood out of the heart (aorta). There is separation of the layers within the aortic wall. Tears in the intimal layer results in the propagation of the dissection (proximally or distally) along the wall of the aorta secondary to blood entering the intima-media space. This can lead to aortic rupture or decreased blood flow (ischemia) to organs.

Fig : Dissection of Aorta

How Cardiac dysfunction, due to any of the above cause, impacts person in their daily living occupational functioning ?

• Cardiac impairments might lead to decrease in functioning of cardiac musculature or  decrease in cardiac output and ejection fraction or insufficient cardiac contractility. This leads to insufficient amount of blood availability for oxygenation and carbon dioxide removal within lungs. To compensate for the impaired function, the unaffected cardiac musculature has to put more efforts in order to fullfill the patient's work demands to complete a task i.e. work of heart is increased compared to premorbid state of person's heart.
• All the above pathological changes affects occupational performance as patients feel early fatigability, breathlessness, syncope, cough, decrease in quality and quantity of work, difficult and slowness in occupational functioning. If the severity of heart condition increases (in acute or chronic stage) then it can lead to sudden cardiac arrest.

 

Thankyou for reading !!!

Dr. Pallavi Khadse-Kolhe, Dr. Sheetal Tatar-Dhande, Dr. Ashwini Sangar