The pathogenesis of acute pulmonary edema associated with hypertension

General Cardiology

The Pathogenesis of Acute Pulmonary Edema Associated With Hypertension

Abstracts

Gandhi SK, Powers JC, Nomeir AM. N Engl J Med 2001;344:17– 22. Study Question: Is acute pulmonary edema associated with marked hypertension related to diastolic dysfunction or to transient systolic dysfunction and/or mitral regurgitation? Methods: Thirty-eight patients (14 men and 24 women; mean age, 67 ⫾ 13 years) with acute pulmonary edema and systolic blood pressure ⬎160 mm Hg had evaluation for ejection fraction and regional function by two-dimensional Doppler echocardiography, both during the acute episode and 1 to 3 days after treatment. Results: The mean systolic blood pressure during the initial echocardiographic examination (200 ⫾ 26 mm Hg) was significantly reduced and was reduced at the time of the follow-up examination (139 ⫾ 17 mm Hg, p ⬍ 0.05). Despite this difference in blood pressure, the left ventricular ejection fraction (0.50 ⫾ 0.15 vs. 0.50 ⫾ 0.13) and regional wall motion index (1.6 ⫾ 0.6 vs. 1.6 ⫾ 0.6) were similar during the acute episode and after treatment. Eighteen patients had a normal ejection fraction (at least 0.50) after treatment with the majority of these patients (16/18) having an ejection fraction of at least 0.50 during the acute episode. Severe mitral regurgitation was not detected in any patient. In the remaining 20 patients with ejection fraction ⬍0.50, there was no difference in the ejection fraction during the acute episode (0.41 ⫾ 0.09) and at follow-up (0.40 ⫾ 0.06, p ⫽ 0.53). Conclusions: Exacerbation of diastolic dysfunction rather that transient systolic dysfunction or mitral regurgitation results in acute pulmonary edema in patients with severe hypertension. Perspective: While this study helps to identify the mechanism of hypertensive pulmonary edema, it has little implications on management. Further, this study should be viewed in the light of the fact that transient mitral regurgitation or systolic dysfunction that may have reversed at the time of the echocardiographic study has not been excluded. Such patients in the acute phase require aggressive reduction of afterload (hypertension) irrespective of systolic or diastolic dysfunction. RM

Cardiovascular Effects of 3,4-Methylenedioxymethamphetamine: A Double-Blind, Placebo-Controlled Trial Lester SJ, Baggott M, Welm S, et al. Ann Intern Med 2000;133: 969 –73. Study Question: To evaluate the acute cardiovascular effects of the psychoactive stimulant 3,4-methylenedioxymethamphetamine (MDMA) by using transthoracic two-dimensional and Doppler echocardiography. Use of MDMA is known to be associated with sudden death and cardiovascular collapse. Methods: Eight healthy adults who self-reported MDMA use were tested in 4 weekly sessions with an ascending-dose of oral MDMA hydrochloride, in a double-blind, placebocontrolled design. Echocardiographic effects of dobutamine (5, 20, and 40 ␮g/kg of body weight per minute) were measured in a preliminary session. A week following the echocardiographic exam, oral MDMA (0.5 and 1.5 mg/kg of body weight) or placebo was administered 1 hour before echocardiographic measurements in three weekly sessions. Heart rate and blood pressure were measured at regular intervals before and after MDMA administration. Echocardiographic measures of stroke volume, ejection fraction, cardiac output and meridional wall stress were obtained 1 hour after MDMA administration and during dobutamine infusions. Results: At a dose of 1.5 mg/kg, MDMA increased mean heart rate (by 28 beats/min), systolic blood pressure (by 25 mm Hg), diastolic blood pressure (by 7 mm Hg) and cardiac output (by 2 L/min) similar to those of dobutamine, 20 and 40 ␮g/kg per minute. Meridional wall stress corrected for ejection fraction, decreased after administration of dobutamine, 40 ␮g/kg per minute but did not change after either dose of MDMA. Conclusions: Modest oral doses of MDMA increase heart rate, blood pressure and myocardial oxygen consumption in a magnitude similar to dobutamine, 20 to 40␮g/kg per minute. However, MDMA has no measurable inotropic effects compared with dobutamine. Perspective: This study provides mechanistic insight into the cardiovascular effects of the recreational drug popularly known as “ecstasy.” It provides an explanation as to why MDMA use may increase the risk of cardiovascular complications during sustained exercise (such as dancing) and with concomitant use of other illicit drugs (cocaine) and other activities associated with increased sympathetic tone. Further, it suggests the potential for the use of beta-blockers in the emergency treatment of MDMA induced cardiovascular instability. RM

Effect of Very Early Angiotensin-Converting Enzyme Inhibition on Left Ventricular Dilation After Myocardial Infarction in Patients Receiving Thrombolysis: Results of a Meta-Analysis of 845 Patients De Kam PJ, Voors AA, van den berg MP, et al. J Am Coll Cardiol 2000;36:2047–53. Study Question: To evaluate the effect of angiotensin-converting enzyme (ACE) inhibition ⬍9 hours after myocardial

ACC CURRENT JOURNAL REVIEW May/Jun 2001

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