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January 1, 1988Hypertension47 citations

Cardiac hypertrophy in hypertension. Repolarization abnormalities elicited by rapid lowering of pressure.

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MPMauro PepiMAMarina AlimentoAMAnna Maltagliati

Structured PICO

Does rapid lowering of blood pressure elicit repolarization abnormalities in patients with primary hypertension and left ventricular hypertrophy?

P
Population
42 patients with primary hypertension, divided into Group 1 (n=28) with normal left ventricular mass index and Group 2 (n=14) with increased left ventricular mass index.
I
Intervention
Rapid lowering of diastolic pressure to between 85 and 90 mm Hg with sublingual nifedipine and nitroprusside.
O
Outcome
Repolarization abnormalities (T wave inversion) on continuous 12-lead electrocardiogram.surrogate

Rapid lowering of blood pressure in hypertensive patients with left ventricular hypertrophy can induce acute repolarization abnormalities, suggesting a potential risk of ischemia when pressure is reduced too quickly.

Abstract

In hypertension, coronary flow is augmented and oxygen balance is adequate despite an increase in coronary resistance. For the maintenance of flow in the presence of and after regression of ventricular hypertrophy, the ratio of pressure and ventricular mass must remain normal. Coronary reserve would be altered if treatment normalized pressure but not ventricular mass or if pressure were lowered too fast. We investigated 42 patients with primary hypertension. In 28 (Group I) left ventricular mass index (by ultrasound) was within the mean value +2 SD (96 + 38 g/m2) of 145 controls and exceeded these values in the remaining 14 patients (Group 2). The diastolic pressure was lowered rapidly to between 85 and 90 mm Hg with two potent vasodilators, nifedipine (sublingually) and nitroprusside, while a 12-lead electrocardiogram was recorded continuously. During both tests, seven patients in Group 2 (responders) showed inversion of normal T waves, in lead I, aVL, and V3-6. These changes waxed and waned in parallel with the pressure fall and recovery and were not attributable to alterations in adrenergic tone, conduction disturbances, variations, or group differences in the QRS axis, QTc interval, heart rate, left ventricular fractional shortening, wall stress, rate of dimension increase in early diastole, or isovolumic relaxation. A ""steal phenomenon'' or passive collapse in compliant coronary lesions during vasodilatation seems unlikely; in fact, patients were free from coronary symptoms, and the electrocardiographic alterations occurred only in seven patients in Group 2, who had a greater left ventricular mass index and required a larger pressure drop to return the diastolic pressure to normal.(ABSTRACT TRUNCATED AT 250 WORDS)

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Cite This Study

Pepi et al. (1988) studied this question.

synapsesocial.com/papers/6a15c011a2352da34782dcf6https://doi.org/10.1161/01.hyp.11.1.84
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Coronary Hemodynamics in Hypertensive Heart Disease1985 · 22 citations
  2. 2Relation between electrocardiographic repolarisation changes and mechanical events in left ventricular hypertrophy.1984 · 15 citations
  3. 3Coronary blood flow in left ventricular hypertrophy: a review of experimental data1982 · 58 citations
  4. 4Nifedipine, a new antihypertensive with rapid action1977 · 249 citations
  5. 5Vasodilator therapy in acute myocardial infarction. A comparison of sodium nitroprusside and nitroglycerin.1975 · 176 citations