We thank Dr. Struthers et al. for their valuable comments on our recent editorial1about the value of brain natriuretic peptide (BNP) in the perioperative prediction of cardiac risk after vascular surgery. The editorial discussed the implications of the recent article by Dr. Mahla et al. 2
In their letter, Dr. Struthers et al. emphasize that an elevated BNP is a marker of diverse cardiac phenotype. These include disorders of the atrium (e.g. , fibrillation, distention), the ventricle (e.g. , hypertrophy, ischemia, dysfunction), and/or a cardiac valve (e.g. , aortic stenosis). They further suggest that perioperative trials designed to reduce cardiac risk in the setting of increased BNP be calibrated to the specific etiologic cardiac phenotype.
This principle for trial design based on BNP makes excellent sense because perioperative intervention (mechanical and/or pharmacologic) will depend on the cardiac phenotypic profile. Mechanical interventions include valve repair/replacement for aortic stenosis and/or angioplasty with possible stenting for coronary syndromes. Pharmacologic interventions include anticoagulation and statins for coronary syndromes as well as angiotensin blockade for left ventricular hypertrophy. Mixed intervention will blend appropriate mechanical and pharmacologic therapies as in the aforementioned examples for coronary syndromes.
This type of clinical trial is already being implemented in the care of patients with cardiac disease. In the perioperative setting, an increase in BNP after coronary artery bypass surgery can trigger refinement of biventricular pacing for optimal ventricular synchronization and consequent significant increase in ejection fraction.3In the ambulatory setting, the trend in BNP over time can assess the outcome of pharmacologic intervention in patients with stable ischemic cardiomyopathy.4
As Dr. Struthers et al. also point out, the combination of BNP and cardiac phenotype will not only stratify cardiac risk, but can also target intervention in patients with no overt cardiac disease. These interventions would aim to reduce future adverse cardiac events.
Again, this type of intervention is already being explored in the therapy of cardiac disease. As an example, angiotensin blockade with valsartan has recently been shown to significantly improve the overall cardiovascular profile in adults with asymptomatic cardiovascular abnormalities.5Furthermore, increased BNP significantly predicted future cardiovascular mortality and morbidity in low-risk patients with stable coronary artery disease and preserved ventricular function (a patient cohort with silent cardiac abnormalities).6
In summary, Dr. Struthers et al. are to be congratulated for further refining the predictive value of perioperative BNP with the role of the associated cardiac phenotype whether symptomatic or not. We anticipate that future trials in this area will be of higher quality and impact as a result.
*Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania. email@example.com