Cardiac Hypertrophy

Cardiac hypertrophy is defined as an abnormal increase in heart muscle mass, reflects a response of myocardium to mechanical stress and various stimuli.

Hypertrophy is derived from the Greek hyper, meaning over, and trophy, meaning abnormal enlargement of a part of organ or excessive growth. Hypertrophy is widely believed to be an adaptive response to increased workload or excessive training. By undergoing hypertrophy, ventricular wall stress remains constant at higher intraventricular pressures.

The primary molecular cause of enlargement of the heart is hypertrophy of myocytes (i.e., enlargement of existing cells, without an increase in the number of cells).

At a molecular level, it has been shown to be a dynamic process during the progression of long-standing hypertrophy to eventual heart failure.

First type, eccentric hypertrophy, in which the precipitating stress is volume overload, is characterized by increased heart-wall thickness and ventricular dilation but addition of sarcomere in series. It is more commonly associated with endurance exercise training (e.g., swimming, cycling, and running) pregnancy, and volume overload.

Second one, concentric hypertrophy, in which the imposed stress is pressure overload, is characterized by an increase in wall thickness with the deposition of new sarcomeres, but the chamber radius may not change. It is most often the result of chronic pressure overload, but is possible to a minor degree with isometric physical training such as weight training, weight and hammer throwing, wrestling and bodybuilding.
Cardiac Hypertrophy

Note: Sarcomere is the basic contractile unit of muscle fiber. Each sarcomere is composed of two main protein filaments—actin and myosin

Hypertensive heart disease

Hypertension is a powerful predictor of cardiovascular mortality and death from all causes. It is a major risk factor for the development of systolic heart failure as well as heart failure in the setting of preserved left ventricular function.

Hypertensive heart disease can be defined as the response of the heart to the afterload imposed on the left ventricle by the progressively increasing arterial pressure and total peripheral resistance.

Severe hypertension may directly damage arterioles and cause atherosclerosis. High blood pressure is also a risk for stroke.

The risk of cardiovascular events is increased two or three times in men and women with hypertension. It is estimated that 14% deaths from coronary heart disease in men and 12% of deaths from coronary heart disease in women are due to hypertension.

Hypertensive heart disease is characterized by increased left ventricular mass leading to left ventricular hypertrophy in the absence of aortic stenosis or hypertrophic cardiomyopathy. Other manifestations include diastolic dysfunction and microvascular changes that cause coronary blood flow abnormalities.

Left ventricular hypertrophy increases the rletaove risk for amrtlaity by twofold in subjects with coronary artery disease and by four fold in those with normal epicardial coronary arteries.

In the development of hypertensive heart disease, myocyte hypertrophy is also associated with apoptosis, collagen deposition, a ventricular fibrosis, with as impairment of coronary hemodynamics as well, thus profoundly influencing functional properties of the left ventricle.
Hypertensive heart disease