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Effects of stiffening of arteries and the cardiac muscle

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The essential features of closely linked human cardiovascular aging and hypertension are changes of non-living and living cardiovascular elements, which cause stiffening of arteries and the cardiac muscle. Using pulse wave velocity (PWV) as the measure, arterial stiffness increases on average 59 % from the age group 18-29 years to the age group => 70 years. However, the stiffening does not become apparent until the third or fourth decade of life. During this period the aorta and proximal elastic arteries expand by around 10 % with each beat of the heart.

This causes first fatigue and then fracture of the elastic lamellae in the highly pulsatile vessels with distension and remodelling. This causes progressive stiffening of the aortic wall. The ill effects of aortic stiffening with age are not apparent in early adult life since brachial systolic and pulse pressures remain stable, or actually may decrease in early adult life, while aortic systolic and pulse pressures progressively increase. A typical increase of 20 % in brachial systolic pressure between 20 and 80 years of life corresponds to a twofold increase in brachial pulse pressure and a three to fourfold increase in aortic pulse pressure.

The extent of brachial pulse pressure rise over 60 years underestimates the three to fourfold increase in aortic pulse pressure and corresponding increase in pulsatile left ventricular load, and in the damaging stresses on the walls of susceptible central arteries in vulnerable organs. When pulsations cannot be cushioned in an elastic aorta, they extend peripherally into the microvasculature, especially into the small arteries of organs with high resting blood flow, notably the brain and kidney. The high pulsatile shear stress dislodges endothelial cells and predisposes to thrombosis and micro-infarction, together with high pulsatile tensile stress tearing the arterial wall and predisposing to micro-rupture. Aging with stiffening of arteries and the cardiac muscle affects coronary perfusion and can induce myocardial ischemia quite independently of atherosclerotic coronary disease.

The increase in aortic pulse pressure associated with arterial stiffening leads to an increase in aortic pressure during systole and decrease in aortic pressure during diastole. Myocardial blood requirement is increased as a consequence of aortic stiffening, and is further increased when such stiffening causes left ventricular hypertrophy. Aortic stiffening reduces pressure throughout diastole, and the capacity to perfuse the left ventricle. Left ventricular hypertrophy and loading can decrease the diastolic period through prolonging systolic contraction and delaying relaxation. A decrease in the diastolic period from 55 % to 45 % of the cardiac cycle can have the same effect as an increase in coronary narrowing from 40 % to 90 %. When the cardiovascular ageing (stiffening of arteries and the cardiac muscle) dependent process progresses over decades it culminates in the disease of old age – where cardiac failure is due to a combination of diastolic and systolic dysfunction, caused by a combination of left ventricular hypertrophy and replacement of muscle by fibrosis tissue, where myocardial ischemia is an issue even in the absence of atherosclerotic coronary disease, and where cardiac disability is commonly associated with cerebral and renal microvascular disease, causing intellectual deterioration and renal failure.

These diseases cause an exponential increase in disability in those who escape mutations and malignancy, and usually cause death before 100 years of age in all societies.


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