Hypertensive Heart Disease

Pathological Changes

The minimal anatomic criteria for the diagnosis of HHD are the following:

  1. Left ventricular hypertrophy (i.e., enlargement of left ventricle) is usually a concentric. This left ventricular becomes an important criteria for the diagnosis of HHD if it is present in the absence of other cardiovascular pathologies that might reasonably induce it.
  2. A history of hypertension: However this definition requires considerable qualification. The study of animal models and clinical studies coupled with endomyocardial biopsies have revealed that demonstrable hypertrophy is a relatively late stage of HHD. Long before it becomes evident, there are more subtle biochemical and ultra structural changes accompanied by functional alterations. In addition, hypertension strongly predisposes to atherosclerosis (hardening of walls of blood vessels) and so most patients with elevated blood pressure have significant coronary atherosclerosis (hardened coronary artery-we know that coronary artery is the artery supplying blood to the heart). The Framingham heart study unequivocally established the relationship between hypertension along and the development of left ventricular hypertrophy. Even mild hypertension (levels greater than 140/90), if sufficiently prolonged, produces left ventricular hypertrophy. Approximately 20 to 25 percent of the population of USA suffers from hypertension of this degree making HHD the second most common form of cardiac disease.

Pathogenesis (Origin and Process of Pathology)

Hypertrophy of the heart is an adoptive response to pressure overload or volume overload. In effect its tends to normalise the systolic stress carried by individual myofilaments within mylocytes. However, when the hypertrophy becomes marked it eventually leads to myocyte injury, heart failure, and cardiac dilation. In hypertension the pathogenesis or the cause of pathology is pressure overload. The pressure stress on the ventricular wall leads to the production within mylocytes of new myofilaments, myofibrils, mitochondria and ribosomes (all are cell organelles) and nuclear enlargement along with enlargement of the cell. Since mitotic division does not occur in adult muscles no new cells are produced. There may, however, be replication of sarcomeres alongside existing sarcomeres contributing to cells widening. Still not understood at the molecular level are the pathways by which physical stress induces the structural changes. But some studies suggest that stress alters the functional activity of protein kinase isoenzymes involved in synthesis of structural proteins. But more than stress may be involved in myofibril enlargement. In animal models it can be shown that adrenergic stimulation by itself can lead to cardiac hypertrophy even with complete control of blood pressure-and of even greater interest, it may do so by activation of the Protooncogene C-myC with ventricular hypertrophy. The heart may maintain an adequate output for decades despite the hypertension. What eventually ushers in the onset of cardiac decompensation remains a mystery. As the heart wall thickens, the oxygen demand is increased and the left ventricular compliance is decreased. The already present coronary atherosclerosis adds an element of ischaemia (lack of blood supply). Whatever the basis diffuse interstitial fibrosis develops along with local myocyte atrophy and degeneration. Moreover, the myofibre enlargement increases the distance for diffusion of oxygen and nutrients from adjacent capillaries. Many speculations have been offered but ultimately the basis for cardiac failure in HHD remains unknown.

The essential morphologic evidence of compensated HHD is

Concentric Hypertrophy

(Hypertrophy without dilatation) of the left ventricular wall without accompanying lesions that might account for it (e.g., aortic valve stenosis, coarctation of the aorta). The thickening of the left ventricular wall is more or less symmetric, increasing the ratio of wall thickness to radius of ventricular chamber and increasing the weight of the heart disproportionately to the increase In size.

During the stages of compensated hypertensive heart disease the left ventricular wall thickness may exceed 2.0 em (2.0 centimetres) and the heart weighs 500 gm. In times the increased thickness of the left ventricular wall imparts a stiffness that impairs diastolic filling and consequently reduces the stroke volume output. The pericardium and valvular leaflets are unaffected. The myocardium is red-brown and homogeneous unless ischaemic heart disease has introduced areas of scarring. With the onset of decompensation there may be dilatation of the ventricular chamber with thinning of the wall and enlargement of the external dimensions of the heart. Microscopically the changes in HHD are subtle and readily missed on routine evaluation. The earliest changes are myocyte enlargement with transverse diameters several times normal. As noted earlier the enlargement reflects an increase in sarcoplasmic elements as well as nuclear enlargement possible with hyperploidy. At a more advanced stage the cellular enlargement becomes somewhat more irregular with variation in the transverse diameter of the individual cells and variation between adjacent cells. The disorganisation becomes more marked with time, and the later stages is marked by regressive alterations with loss of myofibrils, disruption of Z bands, loss of linear array of sarcomeres producing shape angulation of the myocyte, random cell atrophy and death and increased interstitial fibrosis.

Clinical Course

Compensated HHD may be asymptomatic and suspected only in the appropriate clinical setting by ECG or ECHO cardiographic indications of left ventricular enlargement. Other causes of heart hypertrophy must be ruled out. In many patients it comes to attention by the onset of atrial fibrillation or cardiac decomposition with cardiac dilation or both. Often there are other manifestations frequently associated with hypertension (Eg. headache, dizziness, nose-bleeds, postural unsteadiness). Depending on the severity of the hypertension, its duration, the adequacy of therapeutic control and the underlying basis for the hypertension, the patient may enjoy normal longevity to die of unrelated causes, may develop progressive ischaemic heart disease owing to the effects of hypertension on coronary atherosclerosis, may suffer progressive renal damage or cerebrovascular stroke, or may experience progressive heart failure. The risk of sudden cardiac death is also increased. Cardiac failure accounts for only about a third of all deaths among hypertensive subjects. There is substantial evidence that effective control of the hypertension will in time lead to regression of the cardiac hypertrophy. Interestingly some anti-hypertensive agents such as direct acting vasodilators do not lead to reduction inventricular mass, but other agents such as the AGII-converting enzyme inhibitors appear to effectively reduce ventricular mass. Still uncertain is whether these ‘reborn’ hearts will resume completely normal function.