Heart Diseases PDF

The heart 1  ANATOMY AND PHYSIOLOGY Average weight of the heart in an adult male is 300-350 gm while that of an adult female is 250-300 gm The thickness of the right ventricular wall is 0.3 to 0.5 cm while that of the left ventricular wall is 1.3 to 1.5 cm. Wall of the hear...

The heart 1  ANATOMY AND PHYSIOLOGY Average weight of the heart in an adult male is 300-350 gm while that of an adult female is 250-300 gm The thickness of the right ventricular wall is 0.3 to 0.5 cm while that of the left ventricular wall is 1.3 to 1.5 cm. Wall of the heart consists mainly of the myocardium which is covered externally by thin membrane, the epicardium or visceral pericardium, and lined internally by another thin layer, the endocardium. The transport of blood is regulated by cardiac valves: two loose flap-like atrioventricular valves, tricuspid on the right and mitral (bicuspid) on the left; and two semilunar valves with three leaflets each, the pulmonary and aortic valves, guarding the outflow tracts.  MYOCARDIAL BLOOD SUPPLY 1. The anterior descending branch of the left coronary artery, commonly called LAD (left anterior descending coronary) supplies most of the apex of the heart, the anterior surface of the left ventricle, the adjacent third of the anterior wall of the right ventricle, and the anterior two-third of the interventricular septum. 2. The circumflex branch of the left coronary artery, commonly called LCX (left circumflex coronary) supplies the left atrium and a small portion of the lateral aspect of the left ventricle. 3. The right coronary artery, abbreviated as RCA supplies the right atrium, the remainder of the anterior surface of the right ventricle, the adjacent half of the posterior wall of the left ventricle and the posterior third of the interventricular septum.  the conduction system The components of the conduction system include: Sinoatrial (SA) node pacemaker (at the junction of the right atrial appendage and superior vena cava) Atrioventricular (AV) node (located in the right atrium along the atrial septum) Bundle of His, connecting the right atrium to the ventricular septum Subsequent divisions into the right and left bundle branches that stimulate their respective ventricles via further arborization into the Purkinje network  Heart failure Heart failure is defined as the pathophysiologic state in which impaired cardiac function is unable to maintain an adequate circulation for the metabolic needs of the tissues of the body. It may be acute or chronic. The term congestive heart failure (CHF) is used for the chronic form of heart failure in which the patient has evidence of congestion of peripheral circulation and of lungs and edema.  Heart failure Adaptive responses maintaining arterial pressure and vital organ perfusion: Frank-Starling mechanism : Increased preload of dilatation enhances contractility Myocardial hypertrophy with or without chamber dilatation Activation of neurohormonal systems : Norepinephrine, renin – angiotensin – aldosterone axis, and atrial natriuretic factor  Heart failure Systolic failure is defined by insufficient ejection fraction (pump failure), and can be caused by any of the many disorders that damage or derange the contractile function of the left ventricle. Mainly occurs in: IHD, Pressure or volume overload, Dilated cardiomyopathy  Heart failure diastolic failure, the left ventricle is abnormally stiff and cannot relax during diastole. Thus, although cardiac function is relatively preserved at rest, the heart is unable to increase its output in response to increases in the metabolic demands of peripheral tissues (e.g., during exercise). Moreover, because the left ventricle cannot expand normally, any increase in filling pressure is immediately transferred back into the pulmonary circulation, producing rapid onset pulmonary edema ( flash pulmonary edema) Diastolic failure predominantly occurs in patients older than age 65 years and for unclear reasons is more common in women. Hypertension is the most common underlying etiology; diabetes mellitus, obesity, and bilateral renal artery stenosis With: Massive LV hypertrophy, Myocardial fibrosis and amyloidosis, Constrictive pericarditis  Left-sided heart failure Systemic hypertension Mitral or aortic valve disease (stenosis) Ischaemic heart disease Myocardial diseases e.g. cardiomyopathies, myocarditis. Restrictive pericarditis. the major pathologic changes are as under: i) Pulmonary congestion and edema causes dyspnoea and orthopnoea. ii) Decreased left ventricular output causing hypoperfusion and diminished oxygenation of tissues e.g. in kidneys causing ischaemic acute tubular necrosis, in brain causing hypoxic encephalopathy, and in skeletal muscles causing muscular weakness and fatigue.  Morphology: Hypertrophied often dilated left ventricle, with secondary enlargement of left atrium that can lead to fibrillation Enlarged BOXCAR nuclei Lungs : – Pulmonary congestion and edema, perivascular and interstitial transudate Kerlys B lines on X-ray, accumulation of edema fluid in alveolar spaces with hemosiderin laden macrophages (heart failure cells) Dyspnea, orthopnea and paroxysmal nocturnal dyspnea Kidneys: – Low cardiac output reduction in renal perfusion activation of renin-angiotensin-aldosterone system retention of salt and water atrial dilatation and release of natriuretic peptide Brain : – Hypoxic encephalopathy  Right-sided heart failure As a consequence of left ventricular failure. Cor pulmonale in which right heart failure occurs due to intrinsic lung diseases. Pulmonary or tricuspid valvular disease. Pulmonary hypertension secondary to pulmonary thromboembolism. Myocardial disease affecting right heart. Congenital heart disease with left-to-right shunt. the pathologic changes are as under: i) Systemic venous congestion in different tissues and organs e.g. subcutaneous oedema on dependent parts, passive congestion of the liver, spleen, and kidneys, ascites, hydrothorax, congestion of leg veins and neck veins. ii) Reduced cardiac output resulting in circulatory stagnation causing anoxia, cyanosis and coldness of extremities.  Morphology : Liver and spleen – Congestive hepatomegaly: Liver increased in size and weight – Chronic passive congestion of cut surfaces. – Centrilobular necrosis in coexisting left sided failure and hypoxia – Cardiac sclerosis or cirrhosis in severe long standing cases – Congestive splenomegaly – Ascitis Kidneys : – Congestion of the kidney, peripheral edema, azotemia Brain : – Venous congestion and hypoxia of the CNS Pleural and pericardial spaces: – Pleural and pericardial effusions Subcutaneous tissues : – Peripheral edema of dependant portions of the body, especially ankle and pretibial edema. Presacral in bedridden, – Anasarca : Generalized massive edema  CARDIAC HYPERTROPHY an increase in size and weight of the myocardium. It generally results from increased pressure load while increased volume load (e.g. valvular incompetence) results in hypertrophy with dilatation of the affected chamber due to regurgitation of the blood through incompetent valve. CAUSES Left ventricular hypertrophy: i) Systemic hypertension ii) Aortic stenosis and insufficiency iii) Mitral insufficiency iv) Coarctation of the aorta v) Occlusive coronary artery disease vi) Congenital anomalies like septal defects and patent ductus arteriosus vii) Conditions with increased cardiac output e.g. thyrotoxicosis, anaemia, arteriovenous fistulae  CARDIAC HYPERTROPHY Right ventricular hypertrophy: i) Pulmonary stenosis and insufficiency ii) Tricuspid insufficiency iii) Chronic lung diseases e.g. chronic emphysema, bronchiectasis, pneumoconiosis, pulmonary vascular disease etc. iv) Left ventricular hypertrophy and failure of the left ventricle  Pressure (concentric) hypertrophy of left ventricle in hypertension or aortic stenosis, increased wall thickness, with normal or reduced cavity diameter Volume-overloaded ventricles develop hypertrophy with dilatation and increased cavity diameter , seen in mitral or arotic regurgitation CARDIAC HYPERTROPHY  CARDIAC DILATATION Quite often, hypertrophy of the heart is accompanied by cardiac dilatation. Stress leading to accumulation of excessive volume of blood in a chamber of the heart causes increase in length of myocardial fibres and hence cardiac dilatation as a compensatory mechanism. CAUSES i) Valvular insufficiency (mitral and/or aortic insufficiency in left ventricular dilatation, tricuspid and/or pulmonary insufficiency in right ventricular dilatation) ii) Left-to-right shunts e.g. in VSD iii) Conditions with high cardiac output e.g. thyrotoxicosis, arteriovenous shunt iv) Myocardial diseases e.g. cardiomyopathies, myocarditis v) Systemic hypertension.  Congenital heart disease Congenital heart disease is the abnormality of the heart present from birth. It is the most common and important form of heart disease in the early years of life and is present in about 0.5% of newborn children. The incidence is higher in premature infants. Congenital anomalies of the heart may be either shunts (left-to-right or right-to-left), or defects causing obstructions to flow. However, complex anomalies involving combinations of shunts and obstructions are also often present. Dextrocardia is the condition when the apex of the heart points to the right side of the chest  LEFT-TO-RIGHT SHUNTS (ACYANOTIC GROUP) In conditions where there is shunting of blood from left-to- right side of the heart, there is volume overload on the right heart producing pulmonary hypertension and right ventricular hypertrophy. Mainly ASD, VSD, PDA Left-to-Right Shunts – most common Early disease, no cyanosis Late disease… cyanosis Increase pulmonary volume (ASD) and pressure (VSD,PDA) Pulmonary HT  reverse blood flow (Eisenmenger Syndrome) Mutation of TF TBX5  ASD, VSD Mutation of TF NKX2.5  isolated ASD  ATRIAL SEPTAL DEFECT (ASD) Isolated ASD comprises about 10% of congenital heart diseases. Depending upon the location of the defect, there are 3 types of ASD: i) Fossa ovalis type or ostium secundum type is the most common form comprising about 90% cases of ASD. ii) Ostium primum type comprises about 5% cases of ASD. The defect lies low in the interatrial septum adjacent to atrioventricular valves. iii) Sinus venosus type accounts for about 5% cases of ASD. The defect is located high in the interatrial septum near the entry of the superior vena cava. MORPHOLOGIC FEATURES The effects of ASD are as follows: i) Volume hypertrophy of the right atrium and right ventricle. ii) Enlargement and haemodynamic changes of tricuspid and pulmonary valves. iii) Focal or diffuse endocardial hypertrophy of the right atrium and right ventricle. iv) Volume atrophy of the left atrium and left ventricle. v) Small-sized mitral and aortic orifices.  Less likely to close spontaneously In less than 10%  pulmonary HT Paradoxical emboli Irreversible pulmonary vascular disease HF due to mitral insufficiency in ostium primum defects  VENTRICULAR SEPTAL DEFECT (VSD) VSD is the most common congenital anomaly of the heart and comprises about 30% of all congenital heart diseases. Most close spontaneously. Depending upon the location of the defect, VSD may be of the following types: 1. In 90% of cases, the defect involves membranous septum and is very close to the bundle of His. 2. The remaining 10% cases have VSD immediately below the pulmonary valve (subpulmonic), below the aortic valve (subaortic). – reversal of the shunt and cyanosis, occurs earlier and more frequently in patients with VSDs than in those with ASDs; MORPHOLOGIC FEATURES The effects of VSD are as under: i) Volume hypertrophy of the right ventricle. ii) Enlargement and haemodynamic changes in the tricuspid and pulmonary valves. iii) Endocardial hypertrophy of the right ventricle. iv) Pressure hypertrophy of the right atrium. v) Volume hypertrophy of the left atrium and left ventricle. vi) Enlargement and haemodynamic changes in the mitral and aortic valves. PDA  PATENT DUCTUS ARTERIOSUS (PDA) Normally, the ductus closes functionally within the first or second day of life. Its persistence after 3 months of age is considered abnormal. In about 90% of cases, it occurs as an isolated defect, while in the remaining cases it may be associated with other anomalies like VSD, coarctation of aorta and pulmonary or aortic stenosis. MORPHOLOGIC FEATURES The effects of PDA on heart are as follows: i) Volume hypertrophy of the left atrium and left ventricle. ii) Enlargement and hemodynamic changes of the mitral and pulmonary valves. iii) Enlargement of the ascending aorta. High pressure left to right shunt (machinery murmur)  RIGHT-TO-LEFT SHUNTS (CYANOTIC GROUP) In conditions where there is shunting of blood from right side to the left side of the heart, there is entry of poorly-oxygenated blood into systemic circulation resulting in early cyanosis. Hypertrophic osteoarthropathy and polycythemia Paradoxical emboli Tetralogy of Fallot Transposition of great vessels  TETRALOGY OF FALLOT Tetralogy of Fallot is the most common cyanotic congenital heart disease, found in about 10% of children with anomalies of the heart. The four features of tetralogy are as under: i) Ventricular septal defect (VSD) (‘shunt’). ii) Displacement of the aorta to right so that it overrides the VSD. iii) Pulmonary stenosis (‘obstruction’). iv) Right ventricular hypertrophy. V) Right ventricular outflow obstruction  TETRALOGY OF FALLOT The clinical severity largely depends on the degree of the pulmonary outflow obstruction. Boot shaped heart Squatting position (Squatting increases peripheral vascular resistance (PVR) and thus decreases the magnitude of the right-to-left shunt across the ventricular septal defect (VSD)  TRANSPOSITION OF GREAT ARTERIES The term transposition is used for complex malformations as regards position of the aorta, pulmonary trunk, atrioventricular orifices and the position of atria in relation to ventricles. – Incompatible with postnatal life in pure complete form – 35% with VSD – Patent foramen ovale or PDA 65%  OBSTRUCTIONS (OBSTRUCTIVE CONGENITAL HEART DISEASE) Congenital obstruction to blood flow may result from obstruction in the aorta due to narrowing (coarctation of aorta), obstruction to outflow from the left ventricle (aortic stenosis and atresia), and obstruction to outflow from the right ventricle (pulmonary stenosis and atresia). Coarctation of aorta  Coarctation of aorta The word ‘coarctation’ means contracted or compressed. Coarctation of aorta is localised narrowing in any part of aorta, but the constriction is more often just distal to ductus arteriosus (postductal or adult), or occasionally proximal to the ductus arteriosus (preductal or infantile type) in the region of transverse aorta. M>F Females with Turner frequently have coarctation In 50% accompanied by bicuspid aortic valve Infantile form with aortic hypoplasia proximal to PDA – Tubular narrowing of aortic segment between left subclavian artery and patent ductus arteriosus – Cyanosis of the lower half of the body – Weak femoral pulses  Coarctation of aorta Adult form with ridgelike infolding of the aorta – Postductal, ridge of tissue at or just distal of ligamentum arteriosum – Upper extremity HT (poor renal perfusion) – Low pressure on lower extremities – Collateral enlargement of intercostal and mammary arteries (notching of the ribs)  Ischemic heart disease IHD (IHD) is defined as acute or chronic form of cardiac disability arising from imbalance between the myocardial supply and demand for oxygenated blood. IHD is invariably caused by disease affecting the coronary arteries, the most prevalent being atherosclerosis accounting for more than 90% cases, while other causes are responsible for less than 10% cases of IHD. Leading cause of death in males and females in industrialized nations  Ischemic heart disease IHD CORONARY ATHEROSCLEROSIS Coronary atherosclerosis resulting in ‘fixed’ obstruction is the major cause of IHD in more than 90% cases. NON-ATHEROSCLEROTIC CAUSES Several other coronary lesions may cause IHD in the remaining 10% of cases. 1. Vasospasm 2. Stenosis of coronary ostia 3. Arteritis 4. Embolism 5. Thrombotic diseases 6. Trauma 7. Aneurysms 8. Compression  Ischemic heart disease IHD Depending upon the suddenness of onset, duration, degree, location and extent of the area affected by myocardial ischemia, the range of changes and clinical features may range from an asymptomatic state at one extreme to immediate mortality at another: A. Asymptomatic state B. Angina pectoris (AP) C. Acute myocardial infarction (MI) D. Chronic ischemic heart disease (CIHD)/Ischemic cardiomyopathy/ Myocardial fibrosis E. Sudden cardiac death The term acute coronary syndromes include a triad of acute myocardial infarction, unstable angina and sudden cardiac death Acute Plaque Change : Hemorrhage into the atheroma expanding its volume, rupture, fissuring, erosion or ulceration exposing thrombogenic substances  Ischemic heart disease IHD ANGINA PECTORIS Angina pectoris is characterized by paroxysmal and usually recurrent attacks of substernal or precordial chest discomfort caused by transient (15 seconds to 15 minutes) myocardial ischemia that is insufficient to induce myocyte necrosis It is a clinical syndrome of IHD resulting from transient myocardial ischemia. It is characterized by paroxysmal pain in the substernal or precordial region of the chest which is aggravated by an increase in the demand of the heart and relieved by a decrease in the work of the heart. Often, the pain radiates to the left arm, neck, jaw or right arm. It is more common in men past 5th decade of life. Occurs when there is a demand for increased myocardial work, usually through exercise, in the presence of impaired perfusion by blood. The patients with angina show at least one stenosis over 50% of the lumen in a main coronary artery (high-grade stenosis). The high-grade stenosis limits flow when high flow needed such as in exercise. There are 3 overlapping clinical patterns of angina pectoris with some differences in their pathogenesis:  Ischemic heart disease IHD STABLE OR TYPICAL ANGINA Stable (typical) angina is the most common form of angina; it is caused by an imbalance in coronary perfusion (due to chronic stenosing coronary atherosclerosis) relative to myocardial demand, such as that produced by physical activity, emotional excitement or psychological stress. Stable or typical angina is characterized by attacks of pain following physical exertion or emotional excitement and is relieved by rest. The pathogenesis of condition lies in chronic stenosing coronary atherosclerosis that cannot perfuse the myocardium adequately when the workload on the heart increases. UNSTABLE OR CRESCENDO ANGINA Also referred to as ‘pre-infarction angina’ or ‘acute coronary insufficiency’, this is the most serious pattern of angina. It is characterized by more frequent onset of pain of prolonged duration and occurring often at rest. It is thus indicative of an impending acute myocardial infarction. progress to myocardial infarction or may die from secondary development of a ventricular arrhythmia and is caused by fissuring of atherosclerotic plaque Unstable or crescendo angina refers to a pattern of increasingly frequent, prolonged (>20 min), or severe angina or chest discomfort that is described as frank pain, precipitated by progressively lower levels of physical activity or even occurring at rest PRINZMETAL’S VARIANT ANGINA Prinzmetal variant angina is an uncommon form of episodic myocardial ischemia; it is caused by coronary artery spasm. This pattern of angina is characterized by pain at rest and has no relationship with physical activity. The exact pathogenesis of Prinzmetal’s angina is not known. It may occur due to sudden vasospasm of a coronary trunk induced by coronary atherosclerosis, or may be due to release of humoral vasoconstrictors.  Myocardial infarction, also commonly referred to as “heart attack,” is the death of cardiac muscle due to prolonged severe ischemia MI can occur at virtually any age; nearly 10% of myocardial infarcts occur in people younger than age 40, and 45% occur in people younger than age 65.  Pathogenesis -MI Coronary Arterial Occlusion. The following sequence of events likely underlies most MIs A coronary artery atheromatous plaque undergoes an acute change consisting of intraplaque hemorrhage, erosion or ulceration, or rupture or fissuring. When exposed to subendothelial collagen and necrotic plaque contents, platelets adhere, become activated, release their granule contents, and aggregate to form microthrombi. Vasospasm is stimulated by mediators released from platelets. Tissue factor activates the coagulation pathway, adding to the bulk of the thrombus. Within minutes, the thrombus can expand to completely occlude the vessel lumen.  LOCATION OF INFARCTS The region of infarction depends upon the area of obstructed blood supply by one or more of the three coronary arterial trunks. Accordingly, there are three regions of myocardial infarction: 1. Stenosis of the left anterior descending coronary artery is the most common (40-50%). The region of infarction is the anterior part of the left ventricle including the apex and the anterior two- thirds of the interventricular septum. 2. Stenosis of the right coronary artery is the next most frequent (30-40%). It involves the posterior part of the left ventricle and the posterior one-third of the interventricular septum. 3. Stenosis of the left circumflex coronary artery is seen least frequently (15-20%). Its area of involvement is the lateral wall of the left ventricle.  TYPES OF INFARCTS Full-thickness or transmural, when they involve the entire thickness of the ventricular wall. This is the most common type seen in 95% cases. Critical coronary narrowing (more than 75% compromised lumen) is of great significance in the causation of such infarcts. Subendocardial or laminar, when they occupy the inner subendocardial half of the myocardium. These have their genesis in reduced coronary perfusion due to coronary atherosclerosis but without critical stenosis (not necessarily 75% compromised lumen), aortic stenosis or haemorrhagic shock.  TYPES OF INFARCTS Circumferential subendocardial infarction (10% of cases) : involves the subendocardial zone of the ventricle and is caused by a general hypoperfusion of the main coronary arteries. This is usually due to an episode of modest hypotension critically reducing flow in arteries already affected by high-grade atherosclerotic stenosis. The region at the end of the arterial perfusion zone, the subendocardial zone, fails to be perfused and undergoes necrosis  DIAGNOSIS The diagnosis of acute MI is made on the observations of 3 types of features: 1. Clinical features Typically, acute MI has a sudden onset. i) Pain ii) Indigestion iii) Apprehension iv) Shock v) Oliguria vi) Low grade fever vii) Acute pulmonary edema. 2. ECG changes The ECG changes are one of the most important parameters. Most characteristic ECG change is ST segment elevation in acute MI (termed as STEMI); other changes inlcude T wave inversion and appearance of wide deep Q waves. 3. Serum cardiac markers Certain proteins and enzymes are released into the blood from necrotic heart muscle after acute MI. Measurement of their levels in serum is helpful in making a diagnosis and plan management. i) Creatine phosphokinase (CK) and CK-MB CK has three forms— a) CK-MM derived from skeletal muscle; b) CK-BB derived from brain and lungs; and c) CK-MB, mainly from cardiac muscles and insignificant amount from extracardiac tissue.  Sequale of events – Disruption of a plaque thrombus – + vasospasm and platelet aggregation – Necrosis begins within 20-30 min in the subendocardial area _ Extends to midmyocardium – Reaches full size by 3-6 hours – Thrombolytic agents may limit the size of the infarct during that period only  Complications of Myocardial Infarction Short Term Complications of Myocardial Infarction ( within 2 weeks ) – cardiac dysrhythmia, particularly ventricular fibrillation. Bradyarrhythmias are particularly seen with posterior (inferior) infarcts, as the AV node is often involved. – left ventricular failure , most common with very large areas of infarction, which cause cardiac dilatation as the necrotic wall softens in organization.  Complications of Myocardial Infarction – Rupture of the ventricular wall at any time, usually 2-10 days after the infarct, leading to hemopericardium and tamponade Rupture of the septum  acute LR shunt  CHF Papillary muscle dysfunction mitral (or tricuspid) valve incompetence, most post-infarct regurgitation results from ischemic dysfunction of a papillary muscle Mural thrombus formation on the inflamed endocardium over the area of infarction. Fragments can break off and embolize to various organs (particularly the brain, spleen, kidney, gut and lower limbs), producing infarction.  Complications of Myocardial Infarction Long-term complications of myocardial infarction – Chronic intractable left-heart failure. – Ventricular aneurysm formation due to gradual distension of that part of the left ventricular wall – Recurrent myocardial infarction is a risk because of the underlying coronary artery insufficiency – Dressler's syndrome is a form of immune- mediated pericarditis associated with a high ESR. It develops in a very small  CHRONIC ISCHAEMIC HEART DISEASE Chronic ischaemic heart disease, ischaemic cardiomyopathy or myocardial fibrosis, are the terms used for focal or diffuse fibrosis in the myocardium characteristically found in elderly patients of progressive IHD. The patients generally have gradually developing CHF due to decompensation over a period of years. ETIOPATHOGENESIS In majority of cases, coronary atherosclerosis causes progressive ischaemic myocardial damage and replacement by myocardial fibrosis. A small percentage of cases may result from other causes such as emboli, coronary arteritis and myocarditis.  CHRONIC ISCHAEMIC HEART DISEASE The heart may be normal in size or hypertrophied. The left ventricular wall generally shows foci of grey-white fibrosis in brown myocardium. i) There are scattered areas of diffuse myocardial fibrosis, especially around the small blood vessels in the interstitial tissue of the myocardium. ii) Intervening single fibres and groups of myocardial fibres show variation in fibre size and foci of myocytolysis. iii) Areas of brown atrophy of the myocardium may also be present. iv) Coronary arteries show atherosclerotic plaques and may have complicated lesions in the form of superimposed thrombosis.  SUDDEN CARDIAC DEATH defined as sudden death within 24 hours of the onset of cardiac symptoms. The most important cause is coronary atherosclerosis; less commonly it may be due to coronary vasospasm and other non-ischemic causes. The mechanism of sudden death by myocardial ischemia is almost always by fatal arrhythmias, chiefly ventricular asystole or fibrillation. At autopsy, such cases reveal most commonly critical atherosclerotic coronary narrowing (more than 75% compromised lumen) in one or more of the three major coronary arterial trunks with superimposed thrombosis or plaque-haemorrhage. COR PULMONALE ( Pulmonary Heart Disease) – Pulmonary parenchymal or vascular disease  Pulmonary hypertension  disease of right sided cardiac chambers – Acute Mostly PE,  RV dilatation – Chronic Mostly COPD,  hypertrophy then dilatation