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Editorials

Left ventricular hypertrophy

BMJ 1995; 311 doi: https://doi.org/10.1136/bmj.311.7000.273 (Published 29 July 1995) Cite this as: BMJ 1995;311:273
  1. John Chambers, Senior lecturer
  1. Cardiology Guy's Hospital, London SE1 9RT

    An underappreciated coronary risk factor

    Left ventricular hypertrophy is often assumed to be little more than a marker for hypertension. In fact, the relation between diastolic or systolic blood pressure and left ventricular mass is not always close.1 2 Left ventricular hypertrophy is an independent risk factor for myocardial infarction and death in men and women with hypertension3 4 and in asymptomatic subjects with normal blood.5 6 In hypertensive patients it is a stronger coronary risk factor than casual blood pressure readings.

    Early data from the Framingham study showed that patients with ST-T repolarisation abnormalities (“strain”) on the electrocardiogram had a sixfold increase in cardiac deaths over a 20 year follow up period.7

    Echocardiography, however, is 5-10 times more sensitive than the electrocardiogram and detects left ventricular hypertrophy in 25-30% of all hypertensive patients.2 In such patients, myocardial infarction or death occurs at the rate of 4.6 events per 100 patient years, three times the risk in patients with hypertension and normal left ventricular mass.3 Women are not spared this increased risk.4 Even in asymptomatic subjects with normal blood pressure, increased left ventricular mass emerges as a risk factor for coronary disease, cardiac death, and all cause mortality.6 The relative risk of all cause mortality is 1.5 in men and 2.0 in women for every 50 g/m increment in left ventricular mass indexed to height. The relative risk of sudden death is 1.7 per 50 g/m increment.

    In all these studies multivariate analysis shows that, as a risk factor, left ventricular hypertrophy is independent of systolic and diastolic blood pressure, smoking, and cholesterol concentrations.3 4 5 6 It is not always independent of age.4 6 The relation between left ventricular mass and established coronary artery disease has also been examined in black subjects: left ventricular hypertrophy with normal coronary anatomy was associated with a five year mortality of 16.1%, which was similar to the mortality (17.6%) with multivessel disease and normal left ventricular mass. Left ventricular hypertrophy was a more important independent predictor of death than multivessel disease or impaired left ventricular systolic function.8 Other studies have shown a similar effect on the risk of death and reinfarction after Q wave9 or non-Q wave infarction.10

    Care must be taken when applying the results of these studies to individual patients. In routine clinical practice, left ventricular hypertrophy is usually defined by increased wall thickness, while research studies have used M mode echocardiography to estimate left ventricular mass with a formula incorporating septal and posterior wall thickness and diastolic cavity diameter.11 This calculation is then indexed either to height or to body surface area and a threshold for hypertrophy determined by using a control population.

    Definitions of left ventricular hypertrophy have varied and normotensive control subjects may have an incidence from 1.3% to 9.4% according to which one of 13 criteria is applied.2 For research purposes it is probably better to treat left ventricular mass as a continuous variable without categorising it as either normal or abnormal; in clinical use, thresholds for hypertrophy of 134 g/m2 in men and 110 g/m2 in women seem reasonable.2 However, even these may vary with population characteristics such as age, race, and physical activity, so that matched contemporaneous control groups should ideally be used. Furthermore, M mode tends to overestimate left ventricular mass, and two dimensional methods are more accurate, particularly when cavity size or myocardial thickness is non-uniform.12 Generalisation to the whole left ventricle from M mode dimensions recorded at the base of the heart is inappropriate in the presence of established infarction; this diminishes the importance of some studies.8

    What explains the association between left ventricular hypertrophy and increased risk? Although left ventricular mass may correlate poorly with casual systolic blood pressure and even less well with diastolic blood pressure,1 2 it is better related to 24 hour13 or 30 year history of blood pressure.14 Therefore, increased left ventricular mass could still be a marker for end organ effects of long term hypertension. Left ventricular hypertrophy, however, is also known to be determined by other factors that may possibly increase coronary risk—these include obesity, age, blood viscosity, salt intake,1 2 and various genetically determined influences. The dd genotype of the angiotensin converting enzyme gene is linked with left ventricular hypertrophy but not with hypertension and has been shown to carry a higher risk of fatal and non-fatal myocardial infarction than the ii genotype in some15 16 but not all studies.17 Left ventricular hypertrophy may also occasionally develop as a result of established coronary disease as repeated ischaemia in dogs can induce left ventricular hypertrophy.18

    Left ventricular mass may itself contribute to coronary risk through increased oxygen demand and reduced coronary reserve, impaired endocardial autoregulation, and possibly small vessel disease.19 Finally, increased left ventricular mass may result not only from cell hypertrophy but also from increases in collagen, which may provide a substrate for malignant arrhythmias and sudden death.20

    Given the prognostic importance of left ventricular hypertrophy it seems appropriate to look for it in every patient at risk. As left ventricular mass is not closely related to casual blood pressure readings, we need to investigate patients with borderline as well as unequivocal hypertension.

    Several management options exist when left ventricular hypertrophy is detected. We might apply the same aggressive treatment of coronary risk factors as after documented infarction because the risk of future cardiac events is about the same. We could initiate earlier investigation of such patients with routine nuclear imaging or stress echocardiography. Once it is found, we might treat coronary disease more aggressively than usual as even single vessel disease more than doubles mortality if associated with left ventricular hypertrophy.8 Or we could aim for regression of left ventricular hypertrophy as well as blood pressure control by choosing angiotensin converting enzyme inhibitors, nondihydropyridine calcium channel ß blockers, or blockers without intrinsic sympathomimetic activity. In patients with borderline hypertension, left ventricular hypertrophy argues the need for treatment.

    Although all these approaches are intuitively sensible, and unlikely to do harm, none has yet been tested in this group of patients. We need research to guide management in these patients, but until the results are available it seems sensible to use left ventricular hypertrophy as a cue for tighter risk factor management, blood pressure control, and investigation for coexistent coronary artery disease.

    References

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