Table 4 Important predictors of post-response LVEF decline (multivariable logistic regression). Final models adjusted for important clinical characteristics such as age, gender, NYHA class Predictors Post-response LVEF decline (n = 32) Unadjusted Adjusted OR p value OR p value Baseline LVEF (overall) 1.047 0.038 1.075 0.029 Race (white is reference) Hispanic race 3.128 0.003 6.094 <0.001 AA 0.926 0.842 0.595 0.224 NYHA class 1.431 0.240 2.287 0.035 BB dose (low dose of BB is reference)
Medium-dose EX527 BB 1.553 0.259 1.220 0.687 High-dose BB 0.420 0.069 0.312 0.063 ACEI/ARB 0.765 0.738 0.532 0.472 Gender 0.652 0.265 0.951 0.910 Age 0.960 0.005 0.933 <0.001 AA African Americans, ACEI angiotensin-converting enzyme inhibitors, ARB Angiotensin II receptor blockers, BB beta blocker, LVEF left ventricular ejection fraction, NYHA New York Heart Association, OR odds ratio 4 Discussion This study aimed to examine the frequency of decline in LVEF after initial response to BB therapy and to compare this frequency between AA, Hispanic, and Caucasian patients. The primary finding of this study was that there might be a significant proportion of HF patients whose LVEF declines
after initially responding to BB therapy. This conclusion is drawn from the observed occurrence of LVEF decline selleck screening library after initial response to BB therapy at a rate of 13.44 % over 4 years after the initiation of therapy. Compared with other races, Hispanics had lower nadir LVEF (22 %, p < 0.001). Important predictors of LVEF decline were Hispanic race, NYHA class, baseline LVEF, and age, but not gender. In our study, we found that there seems to exist an occurrence of LVEF decline after initial response to BB therapy at a rate of 13.44 % over 4 years after the initiation of therapy in patients with NICM. Prior studies have shown that patients with NICM may respond Phosphatidylinositol diacylglycerol-lyase better to BBs than patients with ischemic cardiomyopathy [26–28]. Patients with NICM have initially increased wall tension due
to dilated LV that causes increased myocardial oxygen demands. The global subendocardial ischemia might form a homogeneous substrate for BB action. Therefore BBs may find a more homogeneous substrate in the first months after initiation of therapy. During therapy and maybe over time because of changes in wall stress, this substrate may change and the effect of BBs in LVEF declines. Another factor that may explain the percentage of post-response LVEF decline in patients with NICM may be genetic variability. Prior studies have shown that patients with certain beta receptor genotypes were associated with better clinical response to BBs compared with others [15, 29–32]. Perhaps the patients with post-response LVEF decline have different polymorphisms than the patients with sustained LVEF response. Future research aimed at see more analyzing polymorphisms among patients with NICM who do not seem to have a sustained response to BBs may yield interesting results.