Hypertensive heart disease (HHD) stems from the increased
demands placed on the heart by hypertension pressure overload + ventricular hypertrophy Most commonly seen in the left heart systemic hypertension Pulmonary hypertension right-sided HHD / cor pulmonale. SYSTEMIC (LEFT-SIDED) HYPERTENSIVE HEART DISEASE
THE MINIMAL CRITERIA FOR THE DIAGNOSIS OF SYSTEMIC
HHD:
left ventricular hypertrophy (usually concentric) in the
absence of other cardiovascular pathology A history or pathologic evidence of hypertension.
The Framingham Study established unequivocally that even
mild hypertension (levels only slightly above 140/90 mm Hg), if sufficiently prolonged, induces left ventricular hypertrophy. Appr 25% of the population of the United States suffers from hypertension
MORPHOLOGY.
Hypertension induces left ventricular pressure overload
hypertrophy Initially without ventricular dilation 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 Heart weight may exceed 500 gm. Increased thickness of the left ventricular wall imparts a stiffness that impairs diastolic fillingleft atrial enlargement.
MICROSCOPICALLY
The earliest change of systemic HHD is an increase in the
transverse diameter of myocytes, which may be difficult to appreciate on routine microscopy. At a more advanced stage variable degrees of cellular and nuclear enlargement become apparent, often accompanied by interstitial fibrosis. The biochemical, molecular, and morphologic changes that occur in hypertensive hypertrophy are similar to those noted in other conditions associated with myocardial pressure overload.
PULMONARY (RIGHT-SIDED) HYPERTENSIVE
HEART DISEASE (COR PULMONALE)
Cor pulmonale, as isolated pulmonary HHD is
frequently called, stems from pressure overload of
the right ventricle
Characterized by:
Right ventricular hypertrophy,
Dilation, Failure secondary to pulmonary hypertension. Disorders of the lungs, especially chronic respiratory diseases such as emphysema, or primary pulmonary hypertension.
PH is most frequently associated with structural
cardiopulmonary conditions that increase pulmonary blood flow or pressure (or both), pulmonary vascular resistance, or left heart resistance to blood flow These include the following: CHRONIC OBSTRUCTIVE OR INTERSTITIAL LUNG DISEASES:
Patients with these diseases have hypoxia as well as
destruction of lung parenchyma and hence have fewer alveolar capillaries. This causes increased pulmonary arterial resistance and, secondarily, elevated pressure. ANTECEDENT CONGENITAL OR ACQUIRED HEART DISEASE:
PH occurs in patients with mitral stenosis, for example,
because of an increase in left atrial pressure that leads to an increase in pulmonary venous pressure and, consequently, to
an increase in pulmonary artery pressure.
Recurrent Thromboemboli:
Patients with recurrent pulmonary emboli may have PH
primarily due to a reduction in the functional cross-sectional area of the pulmonary vascular bed brought about by the obstructing emboli, which, in turn, leads to an increase in pulmonary vascular resistance. CONNECTIVE TISSUE DISEASES:
Several of these diseases (most notably systemic sclerosis)
involve the pulmonary vasculature, leading to inflammation, intimal fibrosis, medial hypertrophy, and PH. OBSTRUCTIVE SLEEP APNEA
A common disorder that is associated with obesity and is now
recognized to be a significant contributor to the development of pulmonary hypertension and cor pulmonate.
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. Normally, the myocytes of the right ventricle are haphazardly arranged and the wall contains transmural fat; in right ventricular hypertrophy, fat in the wall disappears and the myocytes align themselves circumferentially.
CLINICAL COURSE.
Idiopathic PH is most common in women who are 20 to 40
years of age Dyspnea Fatigue Chest pain of the anginal type. Severe respiratory distress, Cyanosis
Right ventricular hypertrophy
Death from decompensated cor pulmonale REFERANCES ROBBINS BASIC PATHOLOGY 8th EDITION Pg =198 199 THANK YOU
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