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(Hypertension. 2008;51:e34.)
© 2008 American Heart Association, Inc.

Letters to the Editor

The J-Point Revisited

Department of Medicine, Mount Sinai School of Medicine, James J. Peters Veterans’ Affairs Medical Center, New York, NY

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

Oh, the diabolical J-curve! Will we ever resolve this issue? Recently, you published a posthoc analysis¹ of data from the Valsartan in Acute Myocardial Infarction Trial that showed, inter alia, that, after a myocardial infarction (MI), a sustained low blood pressure (BP; systolic BP <100 mm Hg on 2 of the post-MI visits at 1, 3, and 6 months) was a marker for bad cardiovascular outcomes. We were also told, incidentally, that this subset of patients had a significantly higher incidence of anterior MI and Q-wave MI and significantly higher maximum creatine kinase values during the MI than those who had normal BPs at 1, 3, and 6 months. In my view, these differences are consistent with the idea of a larger volume of infarcted myocardium, which will do 2 things: increase the risk of cardiovascular death and also produce a greater degree of functional impairment with a lower systolic BP. It is reasonable for the authors to say, therefore, that low BP may be associated with adverse events, but the wrong impression may be generated that somehow the lower BP caused cardiovascular deaths.

The editorialists² are right in saying that very low diastolic BPs may theoretically be associated with increased adverse events as follows: (1) because of ischemia from decreased myocardial perfusion; (2) because large artery stiffness is associated with increased pulse pressure and low diastolic pressures; or (3) as an epiphenomenon, related to an underlying illness, causing increased morbidity or mortality for other reasons. However, . . . [Full Text of this Article]

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