Hypertensive cardiomyopathy

During pregnancy, pregnant women show an increase in left ventricular muscle mass index and a decrease in fractional shortening. When studied with echocardiography, many normal pregnant women show a degree of ''physiologic'' diastolic dysfunction. Schannwell etal. (2001) demonstrated affected LV relaxation with a reduction in peak early diastolic flow and an increase of isovolu-metric relaxation time at 33 weeks gestation in normal pregnant women. In pregnant patients with mild chronic hypertension they showed definite signs of diastolic dysfunction with delayed relaxation noted as early as the beginning of the gestation. Some patients with pregnancy-associated hypertension developed diastolic dysfunction at midgestation, while others only showed this abnormality at term. They concluded that in healthy pregnant women, the increased preload associated with normal pregnancy results in a reversible physiologic left ventricular hypertrophy, a significant alteration in diastolic left ventricular function (disturbed relaxation pattern) and a temporary decrease in the efficacy of systolic function. In women with chronic hypertension, however, there is delayed LV relaxation demonstrable at the beginning of pregnancy and in as many as 50% of cases signs of restrictive cardio-myopathy may develop.

Desai et al. (1996) used echocardiography to show that 25% (4/16) of patients they studied with pulmonary edema and hypertensive crisis in pregnancy had impaired left ventricular systolic function. The remaining 75% (12/16) had abnormal left ventricular diastolic filling.

Diastolic dysfunction in patients with severe hypertension from pre-eclampsia needs to be recognized as a potential cause for fulminant pulmonary edema, cardiac failure and sudden death. It is important that the obstetrician understand that diastolic dysfunction can occur despite normal left ventricular systolic function, and in the face of an elevated blood pressure. Pulmonary edema from diastolic dysfunction occurs frequently with severe hypertension, and ''cardiac failure'' is not always associated with hypotension or a diminished ejection fraction. In fact, up to 40% of hypertensive patients presenting with clinical signs of congestive heart failure have normal systolic left ventricular function. The concept that a pre-eclamptic patient with elevated blood pressure cannot be in cardiac failure needs to be discarded. Likewise, the idea that a pre-eclamptic patient who develops severe pulmonary edema always has peripartum cardiomyopathy should be questioned. Peripartum cardiomyopathy is a distinct entity that carries significant implications for long-term therapy and future pregnancies. Pre-eclamptic women who develop pulmonary edema due to diastolic dysfunction and hypertensive cardiomyopathy should not be labeled as having had peripartum cardiomyopathy. The pathophysiology is different, andinmostcasesof hypertensive cardiomyopathy associated with pre-eclampsia the ejection fraction rapidly returns to normal after treatment of the pre-eclampsia. It is highly unlikely that a pre-eclamptic patient with severely elevated blood pressure who develops pulmonary edema is then delivered and recovers rapidly within 24—48 h has peripartum cardiomyopathy. The most likely diagnosis in this scenario is that of hypertensive cardiomyopathy and diastolic dysfunction. Witlin et al. (1997b) have shown that patients with severe myocardial dysfunction due to peripartum cardiomyopathy are unlikely to regain normal cardiac function on follow-up. In addition, the same group showed that pre-eclamp-sia and chronic hypertension are likely to unmask underlying cardiac abnormalities (Witlin et al., 1997a). In situations where it is unclear why the patient is in pulmonary edema echocardiography can be very useful. Not only does it allow an assessment of the systolic and diastolic function, as well as cardiac output, but the state of filling of the vasculature can also be evaluated. This is especially important in a severely pre-eclamptic patient who may have intravascular dehydration but pulmonary congestion and increased capillary permeability. Mabie etal. (1988) showed that obese women with chronic hypertension are at particular risk of underlying cardiac abnormality and diastolic dysfunction.

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