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Malignant hypertension: cardiac structure and function at presentation and during therapy.

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  • Research Article
  • Medicine


We have studied electrocardiograms, chest radiographs, and digitised apex echocardiograms in 16 patients with malignant hypertension before and after up to six months of antihypertensive treatment and compared them with those of eight patients with severe benign hypertension. Adequate blood pressure reduction was obtained in 14 with resolution of retinopathy, but one patient died and another had poor blood pressure control. Nine had electrocardiographic criteria of left ventricular hypertrophy which did not change with treatment and 10 had lateral ischaemia which resolved in seven. The malignant hypertensives were divided into seven with and nine without a previous hypertensive history. Both groups had normal echocardiographic cavity dimensions, but the former group tended to have hypertrophy (similar to that in benign hypertensives) and the latter did not. After adequate reduction of blood pressure, no change in wall and septal thickness occurred (except in one patient with poor blood pressure control). At entry, malignant hypertensives showed delayed mitral valve opening with significant cavity dimension increase during prolonged isovolumic relaxation, reduced peak rate, and prolonged duration of cavity dimension increase and cavity shape change (inward wall motion) during the upstroke of the apexcardiogram which showed a tall "a" wave. After reduction of blood pressure, though the delay in mitral valve opening persisted, the timing of A2 returned towards normal and the dimension change during the upstroke of the apexcardiogram and the relative height of the "a" wave were reduced but remained significantly different from normal. Some patients without a previous hypertensive history may develop a malignant phase without left ventricular hypertrophy on the electrocardiogram or echocardiogram. They maintain their pump function even with radiological pulmonary oedema, have incoordinate relaxation and contraction, and have abnormal filling. Similar functional abnormalities were found in malignant hypertensives with hypertrophy. Treatment to reduce blood pressure reduces incoordinate contraction, but impaired diastolic function persists as in benign hypertension, suggesting that these abnormalities are the result of altered myocardial properties that may occur without hypertrophy.

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