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Left ventricular hypertrophy as a risk factor: the Framingham experience
1Department of Medicine, Evans Memorial Research Foundation, Boston University School of Medicine, Massachusetts.
Insights
Left ventricular hypertrophy (LVH) is a serious risk factor for heart disease and stroke. Prompt detection and management of LVH can significantly reduce mortality and cardiovascular events.
Area of Science:
- Cardiology
- Cardiovascular Disease Research
Background:
- Left ventricular hypertrophy (LVH) is an ominous risk factor for coronary disease, stroke, and cardiac failure.
- Key determinants include elevated blood pressure, obesity, stature, and glucose intolerance, alongside cardiac valve disease and chronic heart disease (CHD).
Purpose of the Study:
- To highlight the preventable nature of LVH and its significant impact on mortality.
- To emphasize the serious risks associated with electrocardiogram-diagnosed LVH (ECG-LVH) and anatomical LVH.
Main Methods:
- The study reviews trends in LVH prevalence and its association with various risk factors and cardiovascular outcomes.
- It analyzes the prognostic implications of ECG-LVH and anatomical LVH, including mortality rates and cardiovascular event risks.
Main Results:
- Downward trends in LVH prevalence correlate with improved hypertension control, indicating preventability.
- ECG-LVH is a lethal finding associated with high mortality rates and increased risk of sudden death, ventricular ectopy, cardiac failure, stroke, and CHD.
- Both anatomical and ECG-LVH independently increase cardiovascular disease risk, with combined presence conferring a greater risk.
Conclusions:
- LVH is a potent, serious clinical finding that should be actively managed, not considered an adaptive process.
- Reversal of LVH significantly reduces all-cause, cardiovascular, and CHD mortality.
- Early detection and correction of LVH are crucial for mitigating severe cardiovascular outcomes.
Abstract:
Left ventricular hypertrophy (LVH) is one of the less common but ominous risk factors for coronary disease, stroke and cardiac failure. The chief determinants of LVH, aside from age, are elevated blood pressure, obesity, stature and glucose intolerance. Cardiac valve disease and chronic heart disease (CHD) also cause LVH. Downward trends in the prevalence of LVH over four decades indicate that LVH is preventable, and this has coincided with improved hypertension control. When evidence of LVH disappears, the risk of all-cause, cardiovascular and CHD mortality is substantially reduced. Cardiovascular events occur incrementally in relation to left ventricular mass with no discernible critical value identifying pathological hypertrophy. LVH as evidenced by electrocardiogram (ECG-LVH), manifested by repolarization abnormality as well as increased voltage, was a lethal finding; with 5 years, 33% of men and 21% of women were dead. ECG-LVH was associated with ventricular ectopy and a sudden death risk comparable to that of CHD or cardiac failure. ECG-LVH was associated with a 3-15-fold increase of cardiovascular events with greatest risk ratios for cardiac failure and stroke. However, CHD is the predominant clinical sequel. No other risk factor approaches LVH in potency. Anatomical (echocardiographic or X-ray) LVH and ECG-LVH each independently contribute to the risk of cardiovascular disease, and having both confers a greater risk than having either alone. LVH is a clinical finding which should be taken seriously and corrected as soon as detected. It should not be regarded as an innocuous adaptive process, augmenting cardiac function.