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Hypertension. 2008;51:e35
Published online before print March 24, 2008, doi: 10.1161/HYPERTENSIONAHA.108.109975
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(Hypertension. 2008;51:e35.)
© 2008 American Heart Association, Inc.


Letters to the Editor

Response to The J-Point Revisited

Jens Jakob Thune; James Signorovitch

Brigham and Women’s Hospital, Boston, Mass

Lars Kober

Rigshospitalet, Copenhagen, Denmark

Eric J. Velazquez

Duke Clinical Research Institute, Duke University Medical Center, Durham, NC

John J.V. McMurray

Western Infirmary, Glasgow, Scotland

Robert M. Califf

Duke Clinical Research Institute, Duke University Medical Center, Durham, NC

Aldo P. Maggioni

ANMCO Research Center, Florence, Italy

Jean L. Rouleau

Montreal Heart Institute, Montreal, Quebec, Canada

Jonathan Howlett

Queen Elizabeth II Health Sciences Centre, Halifax, Nova Scotia, Canada

Steven Zelenkofske

Lehigh Valley Medical Center, Allentown, Pa

Marc A. Pfeffer; Scott D. Solomon

Brigham and Women’s Hospital, Boston, Mass


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

Dr Rosendorff1 reminds us that blood pressure remains a double-edged sword. We agree entirely that the Valsartan in Acute Myocardial Infarction Trial data suggest that low blood pressure in the postmyocardial infarction (MI) setting may simply reflect reduced systolic function associated with large infarcts and is likely a marker for, rather than a cause of, adverse outcome. These data are consistent with those from the many heart failure trials that have associated lower blood pressure with increased risk.2,3 We interpret these data as suggesting that, for those post-MI survivors who end up resembling the chronic heart failure patient, low blood pressure represents a marker of risk.

We also observed that elevated blood pressure in post-MI survivors in the Valsartan in Acute Myocardial Infarction Trial appears to be associated with increased risk of adverse outcomes.4 In these patients, the most important predictor of post-MI hypertension appears to be pre-MI hypertension, suggesting that the predisposition to hypertension is not attenuated by an infarction. Although Valsartan in Acute Myocardial Infarction Trial enrolled only high-risk MI patients with left ventricular dysfunction, heart failure, or both, in the broader group of MI survivors, the number of persistently hypertensive patients is likely to be large and, thus, should be of particular interest to the hypertension community.

Nevertheless, we need to remain cautious in extrapolating the merits or dangers of blood pressure lowering in this population.5 Although patients with persistent low blood pressure after MI appear to be at increased risk and patients with high blood pressure . . . [Full Text of this Article]