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Is ventricular wall stress rather than left ventricular hypertrophy an important contributory factor to sudden
M A James1, T J MacConnell, J V Jones
1Cardiology Department, Bristol Royal Infirmary, England.
Insights
Left ventricular hypertrophy may not directly cause sudden cardiac death. Instead, underlying abnormal heart wall stress is the likely risk factor, though hypertrophy might offer protection.
Area of Science:
- Cardiology
- Physiology
Background:
- Sudden cardiac death is a major cause of mortality.
- Left ventricular hypertrophy (LVH) is often cited as a risk factor for sudden cardiac death.
- LVH develops as a response to increased cardiac wall stress.
Purpose of the Study:
- To review evidence on left ventricular hypertrophy and wall stress as risk factors for sudden cardiac death.
- To explore the role of abnormal wall stress versus LVH in cardiac mortality.
- To present recent findings on LVH's protective effects against arrhythmia.
Main Methods:
- Review of existing basic and clinical research.
- Analysis of evidence linking LVH and wall stress to sudden cardiac death and arrhythmia.
- Discussion of the challenges in measuring wall stress.
Main Results:
- Raised wall stress, not LVH itself, may be the primary risk factor for sudden cardiac death.
- LVH is a measurable consequence of elevated wall stress.
- Emerging evidence suggests LVH can protect against the arrhythmogenic effects of high wall stress.
Conclusions:
- Abnormal cardiac wall stress is a more probable direct cause of sudden cardiac death than LVH.
- Further research is needed to fully understand the complex relationship between wall stress, LVH, and cardiac arrhythmias.
- LVH may play a protective role, independent of its association with wall stress.
Abstract:
Sudden cardiac death comprises a significant proportion of cardiac mortality in Western society. Left ventricular hypertrophy has been identified by many authors as a possible risk factor for sudden cardiac death, however, left ventricular hypertrophy develops in response to external stimuli on the heart as a means of normalizing wall stress. It is possible that the fundamental abnormalities in wall stress, rather than the left ventricular hypertrophy itself, pose the increased risk of sudden death. Left ventricular hypertrophy, the consequence of raised wall stress, is easy to measure and easy to study and it is understandable why this parameter should have received more attention. Wall stress by contrast is difficult to measure, and worse, is variable throughout the ventricle so that it cannot be measured in a single quantifiable figure. As a consequence, only a limited amount of attention has been paid to wall stress as a possible trigger mechanism for cardiac arrhythmia. However, there is evidence from both basic and clinical research to suggest that raised wall stress may be a risk factor for sudden cardiac death and cardiac arrhythmia. This review discusses the evidence for and against left ventricular hypertrophy and wall stress as risk factors for sudden cardiac death, and also presents recent evidence that left ventricular hypertrophy in isolation can protect the heart against the arrhythmogenic effects of raised wall stress.