Response to The J-Point Revisited
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 appear to be at increased risk, we do not know that lowering blood pressure would be beneficial or, beyond a certain level, deleterious. In other words, despite the apparent J-curve in risk, lowering blood pressure would not necessarily push a patient “along” the J-curve. We agree with Denardo et al6 in their accompanying editorial that our concern about increased risk of hypertension in the post-MI patient and the uncertainly about blood pressure lowering in this setting can only truly be answered with an appropriate clinical trial.
E.J.V., J.J.V.M., R.M.C., J.H., M.A.P., and S.D.S. report having received research funding from Novartis Pharmaceuticals. E.J.V., J.L.R., J.H., M.A.P., and S.D.S. report having served as consultants for or having received honoraria from Novartis Pharmaceuticals. The remaining authors report no conflicts.
Rosendorff C. The J-curve revisited. Hypertension. 2008; 51: e34.
Levy WCM, Mozaffarian DM, Linker DTM, Sutradhar SCP, Anker SDM, Cropp ABP, Anand IM, Maggioni AM, Burton PM, Sullivan MDM, Pitt BM, Poole-Wilson PAM, Mann DLM, Packer MM. The Seattle Heart Failure Model: prediction of survival in heart failure. Circulation. 2006; 113: 1424–1433.
Pocock SJ, Wang D, Pfeffer MA, Yusuf S, McMurray JJV, Swedberg KB, Ostergren J, Michelson EL, Pieper KS, Granger CB, on behalf of the CHARM investigators. Predictors of mortality and morbidity in patients with chronic heart failure. Eur Heart J. 2006; 27: 65–75.
Thune JJ, Signorovitch J, Kober L, Velazquez EJ, McMurray JJV, Califf RM, Maggioni AP, Rouleau JL, Howlett J, Zelenkofske S, Pfeffer MA, Solomon SD. Effect of antecedent hypertension and follow-up blood pressure on outcomes after high-risk myocardial infarction. Hypertension. 2008; 51: 48–54.
Denardo SJ, Anderson RD, Pepine CJ. Blood pressure targets after high-risk myocardial infarction: is it time to update the guidelines? Hypertension. 2008; 51: 26–27.