Intra-Aortic Balloon Counterpulsation in Patients With Chronic Heart Failure and Cardiogenic Shock: Clinical Response and Predictors of Stabilization.

OBJECTIVE: The aim of this work was to characterize the clinical response and identify predictors of clinical stabilization after intra-aortic balloon counterpulsation (IABP) support in patients with chronic systolic heart failure in cardiogenic shock before implantation of a left ventricular assist device (LVAD). BACKGROUND: Limited data exist regarding the clinical response to IABP in patients with chronic heart failure in cardiogenic shock. METHODS: We identified 54 patients supported with IABP before LVAD implantation. Criteria for clinical decompensation after IABP insertion and before LVAD included the need for more advanced temporary support, initiation of mechanical ventilation or dialysis, increase in vasopressors/inotropes, refractory ventricular arrhythmias, or worsening acidosis. The absence of these indicated stabilization. RESULTS: Clinical decompensation after IABP occurred in 23 patients (43%). Both patients who decompensated and those who stabilized had similar hemodynamic improvements after IABP support, but patients who decompensated required more vasopressors/inotropes. Clinical decompensation after IABP was associated with worse outcomes after LVAD implantation, including a 3-fold longer intensive care unit stay and 5-fold longer time on mechanical ventilation (P < .01 for both). Although baseline characteristics were similar between groups, right and left ventricular cardiac power indexes (cardiac power index = cardiac index × mean arterial pressure/451) identified patients who were likely to stabilize (area under the receiver operating characteristic curve = 0.82). CONCLUSIONS: Among patients with chronic systolic heart failure who develop cardiogenic shock, more than one-half of patients stabilized with IABP support as a bridge to LVAD. Baseline measures of right and left ventricular cardiac power, reflecting work performed for a given flow and pressure, may allow clinicians to identify patients with sufficient contractile reserve who will be likely to stabilize with an IABP versus those who may need more aggressive ventricular support.

Association of Isolated Coronary Microvascular Dysfunction With Mortality and Major Adverse Cardiac Events: A Systematic Review and Meta-Analysis of Aggregate Data.

Background The impact of coronary microvascular dysfunction (CMD), as diagnosed by reduced coronary flow reserve, on the outcomes of patients with symptoms of myocardial ischemia and nonobstructive coronary artery disease is poorly understood. We performed a systematic review and meta-analysis of observational studies to determine the association of CMD with outcomes. Methods and Results We searched online databases for studies where coronary flow reserve was measured invasively or noninvasively, clinical events were recorded after determination of coronary flow reserve, and the frequency of those events was reported for patients with and without CMD. The primary outcome was all-cause mortality. The secondary outcome was major adverse cardiac events, including cardiac or cardiovascular death, nonfatal myocardial infarction, cardiac hospitalization, or coronary revascularization. Estimates of effect were calculated from crude event rates with a random-effects model. There were 122 deaths in the 4661 patients without CMD (2.6%) and 183 deaths in the 1970 patients with CMD (9.3%). The odds ratio for mortality in patients with CMD compared with those without CMD was 3.93 (95% CI, 2.91-5.30; P<0.001). There were 167 major adverse cardiac events in the 3742 patients without CMD (4.5%) and 245 events in the 1447 patients with CMD (16.9%). The odds ratio for major adverse cardiac events in patients with CMD compared with those without CMD was 5.16 (95% CI, 2.81-9.47; P<0.001). Conclusions CMD is associated with a nearly 4-fold increase in mortality and a 5-fold increase in major adverse cardiac events. Future studies are needed to identify effective strategies to diagnose and treat CMD.