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Three types of dysfunction of the coronary circulation have been described in experimental models of hypertension associated with left ventricular hypertrophy : (1) reduced coronary reserve, (2) a relative decrease in perfusion of subendocardial layers, (3) a shift to the right, i.e. to higher pressures, of the circulation pressure autoregulation range. These abnormalities are also observed in hypertensive patients, although it is significant that they do not appear to be related to the extent of left ventricular hypertrophy. The exact causes of these abnormalities have yet to be elucidated. Left ventricular hypertrophy does not seem to be an essential factor, although in certain experimental models of hypertension, there does appear to be a mismatch between the development of the coronary vasculature and hypertrophy of the myocytes. The stresses in vessels due to the increase in systolic, and especially intraventricular diastolic pressure can be viewed as additional aggravating factors. The essential abnormalities are structural and/or functional alterations in arterial walls. The structural alterations are reflected by a narrowed lumen due to parietal thickening. This may result from growth of muscle fibres (hypertrophy or hyperplasia) or collagen tissue and/or remodelling of tissues with no overall change in mass. Functionally, the reduced ability of the arteries to stretch, resulting from endothelial alterations may also play a role in the abnormalities observed in hypertensive patients. In our studies, we examined the effect of the antihypertensive drug perindopril on the coronary circulation in the renovascular hypertensive rat (two kidneys-1 clip). We found that this inhibitor of angiotensin converting enzyme (ACE) led to a regression of left ventricular hypertrophy with a return to normal of the coronary reserve. Other studies using either this model or the spontaneously hypertensive rat have also pointed to a beneficial action of ACE inhibitors and other antihypertensive agents on the coronary circulation with reversal of the structural alterations in arterioles. Coronary disease is the main cause of mortality in hypertensive patients. Ironically, antihypertensive therapy has yet to live up to its promise of reducing significantly either the incidence or severity of coronary disease in such patients. Specific alterations of the coronary circulation may account for the relative failure of antihypertensive drugs, despite their proven efficacy in other systems (e.g. stroke prevention). The coronary circulation is unique in certain important respects. It is tightly regulated, maintaining an almost constant flow rate over a wide range of aortic arterial pressures (40-160 mmHg). Extraction of oxygen by the myocardium is almost maximal under resting conditions, and so the circulatory reserve depends almost entirely on the capacity to increase blood flow. This reserve is quite large since there may be a 4 to 5-fold increase in coronary flow rate in response to effort. Another significant detail is that myocardial contraction may lead to an interruption of coronary flow, especially in the deep subendocardial layers, which thus tend to be perfused solely during diastole. This last factor can be seen as the Achilles heel of the coronary circulation, which may be severely limited by myocardial hypertrophy, especially in patients with hypertension.

Left ventricular hypertrophy (LVH), defined as an abnormal increase in left ventricular mass (LVM), is detected by echocardiography in 16-19% of a general population. Its prevalence is strongly associated with age, systolic blood pressure and obesity. In addition to the assessment of LVM, echocardiography allows different forms of left ventricular remodelling in hypertension to be described: eccentric or concentric, and symmetric or asymmetric LVH. The significance of the different forms, however, is not yet well defined. Increased LVM is now recognized as a powerful, independent risk factor for all cardiovascular diseases. This observation is at variance with the general concept that LVH is a useful adaptation of the left ventricle to chronic overload. To explain this paradox, three hypotheses are proposed: LVH serves as a marker, a limited adaptative process, or a pathological process. Each hypothesis implies different therapeutic approaches; thus it is necessary to clarify the reasons why LVH is such an important risk factor.

We report a case of mitochondrial myopathy (MM), assessed by histological and biochemical studies. This illness was diagnosed in a 69-year-old patient with myocardiopathy revealed by ventricular arrhythmias. The originality of this case lies in the patient's age, the mode of onset and the biochemical features (i.e. normal mitochondrial enzymatic complexes but very low respiration when using glutamate as a substrate).

M mode echocardiography is certainly an adequate method to evaluate left ventricular hypertrophy (LVH) regression in hypertensive patients, provided that some important conditions are fulfilled. Left ventricular mass assessment can be made only with non-distorted ventricles, as usually encountered in non-complicated hypertensive patients. The main problem is to limit all sources of variability for serial measurements and all sources of subjectivity in their interpretation. So, we propose some guidelines that should be useful when designing and completing such studies. Two-dimensional echocardiography offers the potential advantage of allowing assessment of left ventricular mass even when the left ventricle is far from its usual shape. However, a standardization of methods and studies of its reproducibility are still required before this method could be recommended in studies of LVH regression.