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Ischemic Heart Disease
By: Shefaa’ Alqa’qa’, MD
• Ischemic heart disease (IHD) represents a group of
pathophysiologically related syndromes resulting from myocardial
ischemia—an imbalance between myocardial supply (perfusion)
and cardiac demand for oxygenated blood.
• In more than 90% of cases, myocardial ischemia results from
reduced blood flow due to obstructive atherosclerotic lesions in
the epicardial coronary arteries; consequently, IHD is frequently
referred to as coronary artery disease (CAD). In addition to coronary
atherosclerosis, myocardial ischemia can be caused by coronary
emboli, myocardial vessel inflammation, or vascular spasm.
• IHD can present as one or more of the following clinical syndromes:
- acute coronary syndromes: - Myocardial infarction (MI)
- Angina pectoris
- Sudden cardiac death (SCD).
- Chronic IHD with heart failure
Pathogenesis : The dominant cause of IHD syndromes is insufficient coronary
perfusion relative to myocardial demand; in the vast majority of cases, this is due to
chronic, progressive atherosclerotic narrowing of the epicardial coronary arteries,
and variable degrees of superimposed acute plaque change, thrombosis, and
vasospasm.
- Stable angina results from increases in myocardial oxygen demand that outstrip the
ability of stenosed coronary arteries to increase oxygen delivery; it is usually not
associated with plaque disruption. Obstructing greater than 75% of vascular cross
sectional area.
- Unstable angina is caused by plaque disruption that results in thrombosis and
vasoconstriction, and leads to severe but transient reductions in coronary blood flow.
In some cases, microinfarcts can occur distal to disrupted plaques due to
thromboemboli. Obstruction of 90% of the cross-sectional area of the lumen.
- Myocardial infarction (MI) is often the result of acute plaque change that induces
an abrupt thrombotic occlusion, resulting in myocardial necrosis.
- Sudden cardiac death may be caused by regional myocardial ischemia that induces a
fatal ventricular arrhythmia.
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.
• The pain itself is likely a consequence of the
ischemia-induced release of adenosine,
bradykinin, and other molecules that stimulate
sympathetic and vagal afferent nerves.
•
•
•
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. Typical angina pectoris is
variously described as a deep, poorly localized pressure, squeezing, or burning
sensation (like indigestion), but unusually as pain, usually relieved by rest
(decreasing demand) or administering vasodilators, such as nitroglycerin and
calcium channel blockers (increasing perfusion).
Prinzmetal variant angina : is an uncommon form of episodic myocardial ischemia;
it is caused by coronary artery spasm. Although individuals with Prinzmetal variant
angina may well have significant coronary atherosclerosis, the anginal attacks are
unrelated to physical activity, heart rate, or blood pressure. Prinzmetal angina
generally responds promptly to vasodilators.
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.
Myocardial Infarction
•
Myocardial infarction, also commonly referred to as “heart attack,” is the death of cardiac muscle due to
prolonged severe ischemia.
•
Incidence and Risk Factors: as atherosclerosis
•
Pathogenesis: 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.
In approximately 10% of cases, transmural MI occurs in the absence of the typical coronary atherothrombosis. In such
situations, other mechanisms may be responsible for the reduced coronary blood flow, including:
Vasospasm; due to platelet aggregation or due to drug ingestion (e.g., cocaine or ephedrine).
Emboli
Ischemia without detectable or significant coronary atherosclerosis and thrombosis may be caused by disorders of
small intramural coronary vessels (e.g., vasculitis), hematologic abnormalities (e.g., sickle cell disease), amyloid
deposition in vascular walls, vascular dissection, marked hypertrophy (e.g., aortic stenosis), lowered systemic
blood pressure (e.g., shock), or inadequate myocardial “protection” during cardiac surgery.
• Myocardial Response
Coronary arterial obstruction diminishes blood flow to a region of myocardium , causing ischemia, rapid
myocardial dysfunction, and eventually—with prolonged vascular compromise— myocyte death. The
anatomic region supplied by that artery is referred to as the area at risk. The outcome depends
predominantly on the severity and duration of flow deprivation .
- The early biochemical consequence of myocardial ischemia is the cessation of aerobic metabolism
within seconds, leading to inadequate production of high-energy phosphates (e.g., creatine phosphate
and adenosine triphosphate) and accumulation of potentially noxious metabolites (e.g., lactic acid).
Because of the exquisite dependence of myocardial function on oxygen and nutrients, myocardial
contractility ceases within a minute or so of the onset of severe ischemia. Such loss of function actually
precipitates heart failure long before myocyte death occurs.
- ultrastructural changes (including myofibrillar relaxation, glycogen depletion, cell and mitochondrial
swelling) also develop within a few minutes of the onset of ischemia.
Nevertheless, these early manifestations of ischemic injury are potentially reversible.
Indeed, experimental and clinical evidence shows that only severe ischemia (blood flow 10% or less of
normal) lasting 20 to 30 minutes or longer leads to irreversible damage (necrosis) of cardiac myocytes.
The earliest detectable feature of myocyte necrosis is the disruption of the integrity of the sarcolemmal
membrane, allowing intracellular macromolecules to leak out of necrotic cells into the cardiac
interstitium and ultimately into the microvasculature and lymphatics. This escape of intracellular
myocardial proteins into the circulation forms the basis for blood tests that can sensitively detect
irreversible myocyte damage, and are important for managing MI.
•
The precise location, size, and specific morphologic features of an acute MI
depend on:
- The location, severity, and rate of development of coronary obstructions due to
atherosclerosis and thromboses.
- The size of the vascular bed perfused by the obstructed vessels.
- The duration of the occlusion.
- The metabolic and oxygen needs of the myocardium at risk.
- The extent of collateral blood vessels
- The presence, site, and severity of coronary arterial spasm
- Other factors, such as heart rate, cardiac rhythm, and blood oxygenation.
Necrosis involves approximately half of the thickness of the myocardium in 2 to 3
hours of the onset of severe myocardial ischemia, and is usually transmural within 6
hours. However, in instances where chronic sublethal ischemia has induced a more
well-developed coronary collateral circulation, the progression of necrosis may
follow a more protracted course (12 hours or longer).
•
Knowledge of the areas of myocardium perfused by the major coronary arteries allows
correlation of specific vascular obstructions with their corresponding areas of myocardial
infarction.
The LAD branch of the left coronary artery supplies most of the apex of the heart, the anterior wall of
the left ventricle, and the anterior two thirds of the ventricular septum.
The coronary artery—either RCA or LCX—that perfuses the posterior third of the septum is
called“dominant”. In a right dominant circulation (present in approximately 80% of individuals), the
RCA supplies the entire right ventricular free wall, the posterobasal wall of the left ventricle, and the
posterior third of the ventricular septum, while the LCX generally perfuses only the lateral wall of the
left ventricle.
Although most hearts have numerous intercoronary anastomoses (collateral circulation), relatively little
blood normally courses through these. However, when a coronary artery is progressively narrowed over
time, blood flows via the collaterals from the high- to the low-pressure circulating causing the channels
to enlarge. Through such progressive dilation and growth of collaterals, stimulated by ischemia, blood
flow is provided to areas of myocardium that would otherwise be deprived of adequate perfusion.
The frequencies of involvement of each of the three main arterial trunks are as follows:
Left anterior descending coronary artery (40% to 50%)
Right coronary artery (30% to 40%)
Left circumflex coronary artery (15% to 20%)
•
Patterns of Infarction. The distribution of myocardial necrosis correlates with the location and cause of the
decreased perfusion:
Transmural infarction: Myocardial infarcts caused by occlusion of an epicardial vessel are typically transmural—the
necrosis involves virtually the full thickness of the ventricular wall in the distribution of the affected coronary. This
pattern of infarction is usually associated with a combination of chronic coronary atherosclerosis, acute plaque change,
and superimposed thrombosis .
Subendocardial (nontransmural) infarction: As the subendocardial zone is normally the least perfused region of
myocardium, this area is most vulnerable to any reduction in coronary flow. A subendocardial infarct— typically
involving roughly the inner third of the ventricular wall—can occur as a result of a plaque disruption followed by a
coronary thrombus that becomes lysed (therapeutically or spontaneously) before myocardial necrosis extends across
the full thickness of the wall. Subendocardial infarcts can also result from prolonged, severe reduction in systemic
blood pressure, as in shock superimposed on chronic, otherwise noncritical, coronary stenoses. In the subendocardial
infarcts that occur as a result of global hypotension, myocardial damage is usually circumferential, rather than being
limited to the distribution of a single major coronary artery.
Multifocal microinfarction: This pattern is seen when there is pathology involving only smaller intramural vessels. This
may occur in the setting of microembolization, vasculitis, or vascular spasm. Elevated levels of catechols also increase
heart rate and myocardial contractility, exacerbating ischemia caused by the vasospasm for example, due to drugs
(cocaine) . The outcome of such vasospasm can be sudden cardiac death (usually caused by a fatal arrhythmia) or an
ischemic dilated cardiomyopathy, so-called takotsubo cardiomyopathy (also called “broken heart syndrome” because
of the association with emotional duress).
Owing to the characteristic electrocardiographic changes resulting from myocardial ischemia or necrosis in various
distributions, a transmural infarct is sometimes referred to as an “ST elevation myocardial infarct” (STEMI) and a
subendocardial infarct as a “non–ST elevation infarct” (NSTEMI). Depending on the extent and location of the vascular
involvement, microinfarctions show nonspecific changes or can even be electrocardiographically silent
The gross and microscopic appearance of an infarct depends on the duration
of survival of the patient following the MI.
Early morphologic recognition of acute MI can be difficult, particularly when
death occurs within a few hours of the onset of symptoms. MIs less than 12
hours old are usually not apparent on gross examination. However, if the
infarct preceded death by 2 to 3 hours, it is possible to highlight the area of
necrosis by immersion of tissue slices in a solution of triphenyltetrazolium
chloride. This gross histochemical stain imparts a brick-red color to intact,
noninfarcted myocardium where lactate dehydrogenase activity is preserved.
Because dehydrogenases leak out through the damaged membranes of dead
cells, an infarct appears as an unstained pale zone . By 12 to 24 hours after
infarction, an MI can usually be identified grossly as a reddish-blue area of
discoloration caused by stagnated, trapped blood. Thereafter, the infarct
becomes progressively more sharply defined, yellow tan, and soft. By 10
days to 2 weeks, it is rimmed by a hyperemic zone of highly vascularized
granulation tissue. Over the succeeding weeks, the injured region evolves to
a fibrous scar.
The histopathologic changes also proceed in a fairly predictable sequence. The typical
changes of coagulative necrosis become detectable in the first 6 to 12 hours. The
necrotic muscle elicits acute inflammation (most prominent between 1 and 3 days).
Thereafter, macrophages remove the necrotic myocytes (most noticeable by 3 to 7
days), and the damaged zone is progressively replaced by the ingrowth of highly
vascularized granulation tissue (most prominent at 1 to 2 weeks); as healing
progresses, this is replaced by fibrous tissue. In most instances, scarring is well
advanced by the end of the sixth week, but the efficiency of repair depends on the
size of the original lesion, as well as the relative metabolic and inflammatory state of
the host.
Since healing requires the participation of inflammatory cells, immune suppression
(e.g., due to steroids) can impair the vigor of the healing response. Moreover,
delivering inflammatory cells to the site of necrosis requires intact vasculature; since
blood vessels often survive only at the edges of an infarct, MIs typically heal from the
margins toward the center. Consequently, a large infarct may not heal as quickly or as
completely as a small one. A healing infarct can also appear nonuniform, with the
most advanced healing at the periphery. Once a lesion is completely healed, it is
impossible to determine its age (i.e., the dense fibrous scar of 8-week-old and 10year-old infarcts looks virtually identical).
Infarct Modification by Reperfusion:
• Reperfusion is the restoration of blood flow to ischemic myocardium threatened
by infarction; the goal is to salvage cardiac muscle at risk and limit infarct size.
• This can be accomplished by a host of coronary interventions, that is,
thrombolysis, angioplasty, stent placement, or coronary artery bypass graft [CABG]
surgery. The goal is to dissolve, mechanically alter, or bypass the lesion that
precipitated the acute infarction.
• Reperfused infarcts are usually hemorrhagic because the vasculature is injured
during ischemia and there is bleeding after flow is restored.
• Reperfusion can trigger deleterious complications, including arrhythmias as well
as damage superimposed on the original ischemia, so-called reperfusion injury.
Reperfusion injury may be mediated by oxidative stress, calcium overload, and
inflammatory cells recruited after tissue reperfusion. Reperfusion-induced
microvascular injury not only results in hemorrhage but can also cause endothelial
swelling that occludes capillaries and may limit the reperfusion of critically injured
myocardium (called no-reflow). Stunned myocardium, a state of prolonged cardiac
failure induced by short-term ischemia that usually recovers after several days.
Myocardium that is subjected to chronic, sublethal ischemia may also enter into a
state of lowered metabolism and function called hibernation.
•
Clinical Features:
Patients with MI classically present with prolonged (more than 30 minutes) chest pain described as crushing, stabbing,
or squeezing, associated with a rapid, weak pulse; profuse sweating (diaphoresis), and nausea and vomiting are
common, Dyspnea, 25% of patients the onset is entirely asymptomatic.
The most sensitive and specific biomarkers of myocardial damage are cardiac-specific proteins, particularly cTnT and
cTnI (proteins that regulate calcium-mediated contraction of cardiac and skeletal muscle). Troponins I and T are not
normally detectable in the circulation. Following an MI, levels of both begin to rise at 3-12 hours; cTnT levels peak
somewhere between 12-48 hours while cTnI levels are maximal at 24 hours.
Creatine kinase is an enzyme expressed in brain, myocardium, and skeletal muscle; it is a dimer composed of two
isoforms designated “M” and “B.” While MM homodimers are found predominantly in cardiac and skeletal muscle,
and BB homodimers in brain, lung, and many other tissues, MB heterodimers are principally localized to cardiac
muscle (with considerably lesser amounts found in skeletal muscle). Thus, the MB form of creatine kinase (CK-MB) is
sensitive but not specific, since it can also be elevated after skeletal muscle injury. CK-MB begins to rise within 3 to
12 hours of the onset of MI, peaks at about 24 hours, and returns to normal within approximately 48 to 72 hours.
To summarize:
• Time to elevation of CKMB, cTnT and cTnI is 3 to 12 hrs
• CK-MB and cTnI peak at 24 hours
• CK-MB returns to normal in 48-72 hrs, cTnI in 5-10 days, cTnT in 5 to 14 days
•
Consequences and Complications of Myocardial Infarction:
The risk of postinfarct complications and the prognosis of the patient depend primarily on the infarct size, location, and
fraction of the wall thickness involved. Half of the deaths associated with acute MI occur within 1 hour of onset, most
commonly due to a fatal arrhythmia. anterior transmural infarcts are at greatest risk for free-wall rupture, expansion,
mural thrombi, and aneurysm. In contrast, posterior transmural infarcts are more likely to be complicated by
conduction blocks
- Contractile dysfunction: “pump failure” (cardiogenic shock) occurs in 10% to 15% of patients following acute MI,
generally with large infarcts involving more than 40% of the left ventricle. Cardiogenic shock has a nearly 70% mortality
rate. Right ventricular infarcts can cause right-sided heart Failure
Arrhythmias: include sinus bradycardia, atrial fibrillation, heart block, tachycardia, ventricular premature
contractions, ventricular tachycardia, and ventricular fibrillation. Because of the location of portions of the
atrioventricular conduction system (bundle of His) in the inferoseptal myocardium, infarcts involving this site can
also be associated with heart block.
Myocardial rupture: Rupture of the ventricular free wall (most common), with hemopericardium and cardiac
tamponade. Rupture of the ventricular septum (less common), leading to an acute VSD and left-to-right shunting.
Papillary muscle rupture (least common), resulting in the acute onset of severe mitral regurgitation.
Ventricular aneurysm: bounded by myocardium that has become scarred.
Pericarditis: A fibrinous or fibrinohemorrhagic pericarditis usually develops about the second or third day
following a transmural infarct as a result of underlying myocardial inflammation (Dressler syndrome).
Mural thrombus
Papillary muscle dysfunction: Although papillary muscle rupture after an MI may certainly result in precipitous
onset of mitral (or tricuspid) valve incompetence, most post-infarct regurgitation results from ischemic
dysfunction of a papillary muscle (and underlying myocardium), or later from ventricular dilation or from papillary
muscle fibrosis and shortening.
Progressive late heart failure (chronic IHD)
• The noninfarcted segments of the ventricle undergo hypertrophy
and dilation; collectively, these changes are termed ventricular
remodeling. The compensatory hypertrophy of noninfarcted
myocardium is initially hemodynamically beneficial. However, this
adaptive effect may be overwhelmed by ventricular dilation (with
or without ventricular aneurysm) and increased oxygen demand,
which can exacerbate ischemia and depress cardiac function. There
may also be changes in ventricular shape and stiffening of the
ventricle due to scar formation and hypertrophy that further
diminish cardiac output.
• Long-term prognosis after MI depends on many factors, the most
important of which are the residual left ventricular function and the
extent of any vascular obstructions in vessels that perfuse the
remaining viable myocardium. The overall total mortality within the
first year can be as high as 30%; thereafter, each passing year is
associated with an additional 3% to 4% mortality among survivors.
Chronic Ischemic Heart Disease
• The designation chronic IHD (often called ischemic cardiomyopathy
by clinicians) is used here to describe progressive congestive heart
failure as a consequence of accumulated ischemic myocardial
damage and/or inadequate compensatory responses. In most
instances there has been prior MI and sometimes previous
coronary arterial interventions and/or bypass surgery. Chronic IHD
usually appears postinfarction due to the functional
decompensation of hypertrophied noninfarcted myocardium .
However, in other cases severe obstructive coronary artery disease
may present as chronic congestive heart failure in the absence of
prior infarction.
• MORPHOLOGY: Hearts from patients with chronic IHD have
cardiomegaly, with left ventricular hypertrophy and dilation.
Microscopic findings include myocardial hypertrophy, diffuse
subendocardial vacuolization, and fibrosis.
Sudden Cardiac Death (SCD)
•
SCD is most commonly defined as unexpected death from cardiac causes either without symptoms, or within 1 to
24 hours of symptom onset. Coronary artery disease is the leading cause of SCD, responsible for 80% to 90% of
cases; unfortunately, SCD is often the first manifestation of IHD. There is typically only chronic severe
atherosclerotic disease; acute plaque disruption is found in only 10% to 20% of cases. Healed remote MIs are
present in about 40%.
•
With younger victims, other nonatherosclerotic causes are more common etiologies for SCD:
- Hereditary or acquired abnormalities of the cardiac conduction system
- Congenital coronary arterial abnormalities
- Mitral valve prolapse
- Myocarditis or sarcoidosis
- Dilated or hypertrophic cardiomyopathy
- Pulmonary hypertension
- Myocardial hypertrophy. Increased cardiac mass is an independent risk factor for SCD (e.g athletes)
- Other miscellaneous causes, such as pericardial tamponade, pulmonary embolism, systemic metabolic and
hemodynamic alterations, catecholamines, and drugs of abuse, particularly cocaine and methamphetamine.
The mechanism of SCD is most often a lethal arrhythmia (e.g., asystole or ventricular fibrillation). Notably, infarction
need not occur. 80% to 90% of patients who suffer SCD but are successfully resuscitated do not show any enzymatic or
ECG evidence of myocardial necrosis—even when the original cause was ischemic heart disease. Although ischemic
injury (and other pathologies) can directly affect the major components of the conduction system, most cases of fatal
arrhythmia are triggered by electrical irritability of myocardium distant from the major elements of the conduction
system.
• MORPHOLOGY:
Marked coronary atherosclerosis with a critical (>75%
crosssectional area) stenosis involving one or more of the
three major vessels is present in 80% to 90% of SCD victims;
only 10% to 20% of cases are of nonatherosclerotic origin.
Usually there are high-grade stenoses (>90% of area); in
approximately one half, acute plaque disruption is observed,
and in approximately 25% diagnostic changes of acute MI are
seen. This suggests that many patients who die suddenly are
suffering an MI, but the short interval from onset to death
precludes the development of diagnostic myocardial changes.
Hypertensive Heart Disease
• Hypertensive heart disease (HHD) is a
consequence of the increased demands
placed on the heart by hypertension, causing
pressure overload and ventricular
hypertrophy. Although most commonly seen
in the left heart as the result of systemic
hypertension, pulmonary hypertension can
cause right-sided HHD, or cor pulmonale.
Systemic (Left-Sided) Hypertensive
Heart Disease
Hypertrophy of the heart is an adaptive response to the pressure overload of chronic
hypertension. However, such compensatory changes may be ultimately maladaptive
and can lead to myocardial dysfunction, cardiac dilation, CHF, and in some cases
sudden death. The minimal pathologic criteria for the diagnosis of systemic HHD are
the following:
(1) left ventricular hypertrophy (usually concentric) in the absence of other
cardiovascular pathology
and (2) a clinical history or pathologic evidence of hypertension in other organs (e.g.,
kidney).
MORPHOLOGY:
Hypertension induces left ventricular pressure overload hypertrophy, initially without
ventricular dilation. As a result, the left ventricular wall thickening increases the
weight of the heart disproportionately to the increase in overall cardiac size. The
thickness of the left ventricular wall may exceed 2.0 cm, and the heart weight may
exceed 500 gm. In time the increased thickness of the left ventricular wall, often
associated with increased interstitial connective tissue, imparts a stiffness that impairs
diastolic filling, frequently with consequent left atrial enlargement.
•
Compensated systemic HHD may be asymptomatic, producing only
electrocardiographic or echocardiographic evidence of left ventricular
enlargement. In many patients, systemic HHD comes to attention due to new atrial
fibrillation induced by left atrial enlargement, or by progressive CHF. Depending on
the severity, duration, and underlying basis of the hypertension, and on the
adequacy of therapeutic control, the patient may:
(1) enjoy normal longevity and die of unrelated causes,
(2) develop IHD due to both the potentiating effects of hypertension on coronary
atherosclerosis and the ischemia induced by increased oxygen demand from the
hypertrophic muscle,
(3) suffer renal damage or cerebrovascular stroke as direct effects of hypertension, or
(4) experience progressive heart failure or SCD.
Effective control of hypertension can prevent cardiac hypertrophy, or can lead to its
regression; with normalization of the blood pressure, the associated risks of HHD are
diminished.
Pulmonary (Right-Sided) Hypertensive Heart
Disease (Cor Pulmonale)
• Normally, because the pulmonary vasculature is the low
pressure side of the circulation, the right ventricle has a
thinner and more compliant wall than the left ventricle.
Isolated pulmonary HHD, or cor pulmonale, stems from
right ventricular pressure overload. Chronic cor pulmonale
is characterized by right ventricular hypertrophy, dilation,
and potentially right-sided failure. Typical causes of chronic
cor pulmonale are disorders of the lungs, especially chronic
parenchymal diseases such as emphysema, and primary
pulmonary hypertension. Acute cor pulmonale can follow
massive pulmonary embolism. Nevertheless, it should also
be remembered that pulmonary hypertension most
commonly occurs as a complication of left-sided heart
disease.
• MORPHOLOGY:
In acute cor pulmonale there is marked dilation of the right ventricle
without hypertrophy. On cross-section the normal crescent shape of
the right ventricle is transformed to a dilated ovoid. In chronic cor
pulmonale the right ventricular wall thickens, sometimes up to 1.0 cm
or more. More subtle right ventricular hypertrophy may take the form
of thickening of the muscle bundles in the outflow tract, immediately
below the pulmonary valve, or thickening of the moderator band, the
muscle bundle that connects the ventricular septum to the anterior
right ventricular papillary muscle. Sometimes, the hypertrophied right
ventricle compresses the left ventricular chamber, or leads to
regurgitation and fibrous thickening of the tricuspid valve.
There is commonly right ventricular and right atrial hypertrophy;
right ventricular and atrial dilation can occur.