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The heart in the hypertensive elderly
1Department of Gerontology and Family Medicine, Cracow, Poland.
Insights
Left ventricular hypertrophy (LVH) increases cardiovascular risk in the elderly. Reducing LV mass through treatment, particularly with ACE inhibitors, can improve heart function and prognosis.
Area of Science:
- Cardiology
- Gerontology
- Pathology
Background:
- Left ventricular (LV) mass increases with age, particularly in senescence.
- In normotensive elderly, LVH stems from connective tissue degeneration; in hypertensive patients, it involves muscle and fibrotic tissue increase.
- LVH affects up to 50% of elderly hypertensive patients and is linked to increased cardiovascular events.
Purpose of the Study:
- To investigate the implications of LVH in the elderly.
- To explore the relationship between LVH, aging, and cardiovascular outcomes.
- To evaluate the potential benefits of LVH regression on cardiac function and prognosis.
Main Methods:
- The study reviews existing literature on LV mass, LVH, and aging.
- Echocardiographic criteria are used to define LVH.
- The impact of LVH on coronary reserve, arrhythmias, and LV function is discussed.
Main Results:
- LVH is associated with reduced coronary reserve, increased arrhythmias, and worsened LV function, even without coronary stenosis.
- Increased interstitial fibrosis and collagen cross-linking contribute to myocardial stiffness and diastolic dysfunction in senescent hearts.
- Regression of LVH improves LV filling, coronary reserve, and reduces arrhythmias.
Conclusions:
- LVH regression is associated with improved cardiovascular prognosis and should be a therapeutic goal in hypertension management.
- Angiotensin-converting-enzyme inhibitors show the greatest efficacy in reducing LV mass compared to other antihypertensive agents.
Abstract:
Left ventricular (LV) mass progressively increases throughout life, reaching its greatest magnitude in senescence. In the normotensive elderly, left ventricular hypertrophy (LVH) is mostly a consequence of a degenerative process in connective tissue. In hypertensive patients, LVH results from an increase in muscle mass and fibrotic tissue. LVH by echocardiographic criteria can be found in up to 50% of elderly patients with hypertension. Although associated with aging, LVH is associated with a higher rate of non-fatal and fatal cardiovascular events. Even in the absence of coronary stenosis, LVH is associated with reduced coronary reserve, increased number of arrhythmias and progressive deterioration in LV function. Conceivably, an increase in interstitial fibrosis and cross-linking collagen in the senescent heart is responsible for an increase in myocardial stiffness and diastolic abnormalities. Regression of LVH has been demonstrated not only to improve left ventricular filling and coronary reserve but also to diminish cardiac arrhythmias. Although few studies have demonstrated that the reduction of LV mass is associated with better cardiovascular prognosis, it seems reasonable to consider it a goal of antihypertensive therapy. Of all anti-hypertensive agents, angiotensin-converting-enzyme inhibitors seem to be the most powerful in reducing LV mass.