Search

Background: The interactions between ultrasound and cardiac muscle can be exploited to characterize abnormalities of myocardial structure in echocardiography. Two different methods permit an objective assessment of myocardial tissue characterization: analysis of the radiofrequency signal and videodensitometry. We conducted a videodensitometric study using a new practical semiautomatic software applied on digital signal to evaluate gray level cyclic variations of myocardial walls. The aim was to determine parameters differentiating healthy and hypertrophic myocardium in hypertensive patients. Methods and results: Echocardiographic examinations were performed on 30 hypertensives vs 30 healthy controls using second harmonic imaging. Dynamic 2D sequences were recorded in digital form and transferred on computer. Region of interest (ROI) was selected on interventricular septum (IVS) and the software automatically analyzed its systolo-diastolic displacements. ROI echo intensity and its cyclic variations were computed. Values were normalized with blood backscatter. The hypertensives had a smaller amplitude of gray level cyclic variation than did the controls (22 � 6v s 27� 11; P ¼ 0:02), and this parameter was correlated in multivariate analysis with left ventricle fractional shortening (P ¼ 0:032) and diastolic pressure (P ¼ 0:014). Conclusions: Magnitude of gray level cyclic variation of IVS can be studied easily with this new semi-automatic software, is altered in hypertensives and correlated with parameters of systolic function. (Eur J Echocardiography 2003; 4: 292–299)

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).