Predictors of Appropriate Implantable Cardioverter-Defibrillator Therapy in Patients with Idiopathic Dilated Cardiomyopathy

Evaluating predictors of appropriate implantable cardioverter-defibrillator (ICD) therapy in patients with idiopathic dilated cardiomyopathy (IDC) may be helpful in developing risk stratification strategies for these patients. Fifty-four patients with IDC underwent ICD implantation and were followed up. Twenty-three patients (42%) had a class I indication for ICD implantation; the remaining patients underwent implantation for multiple risk factors for sudden death including left ventricular dysfunction, nonsustained ventricular tachycardia, syncope, or positive electrophysiologic study results. Clinical, electrocardiographic, and electrophysiologic data were collected. Appropriate ICD therapy was defined as an antitachycardia pacing therapy or shock for tachyarrhythmia determined to be either ventricular tachycardia or ventricular fibrillation. Appropriate ICD therapy was observed in 23 patients (42%). There was a significant difference in use of β-blocker therapy between patients who did and did not have appropriate ICD therapy (p <0.0003). Cox regression analysis identified the following univariate predictors (p <0.1): class I indication (p <0.005) and lack of use of β-blocker therapy (p <0.0007). In multivariate analysis, only lack of β-blocker use (relative risk 0.15, 95% confidence intervals 0.05 to 0.45; p <0.0007) was identified as a predictor of appropriate ICD therapy. Of the patients who received ICD therapy, only 4 (17%) were taking β blockers, whereas 21 of the 31 patients (68%) who did not receive ICD therapy were treated with β blockers (p <0.0003). In patients with IDC selected for ICD implantation, the most consistent predictor of appropriate ICD therapy was lack of β-blocker use. Attempts should be made to administer β blockers to these patients, if tolerated

Impaired myocardial perfusion score and inflammatory markers in patients undergoing primary angioplasty for acute myocardial infarction

Background: Microcirculatory dysfunction during acute myocardial infarction is mediated by various mechanisms including inflammation, thrombus, or plaque embolization. We hypothesize that patients with acute myocardial infarction and admission Thrombolysis in Myocardial Infarction (TlMl) myocardial perfusión grade (TMP) &lt; 2 had increased inflammatory status as measured by high sensitivity C-reactive protein (hs-CRP). Methods: From January 2002 to December 2003, 166 patients (178 lesions) were referred for primary percutaneous coronary intervention. Patients were stratified based on pre-PCI TMP &lt; 2 or TMP ³ 2. Univariate and multi-variate predictors of in-hospital and 30-day death were determined with logistic regression. Results: Pre-PCI TMP &lt; 2 was found in 66% vs 34% with TMP ³ 2 (P < .001). Hs-CRP levels were high in both groups but not significantly different (37.9 ± 6 vs 33.7 ± 6 mg/L, P = .63). Patients with TMP &lt; 2 had higher WBC (12.83 ± 4.55 * 10³ vs 10.83 ± 3.00 * 10³, P = .04), lower ejection fraction (40 ± 11% vs 46 ± 12%, P < .001), and higher admission CK-MB levels (116 ± 13 ng/mL vs 55 ± 13 ng/mL, P = .006). Death occurred in 12% in the poor TMP group vs 1.8% in the good TMP group (P = .03). Advanced age, use of an intra-aortic balloon pump, and elevated admission WBC were independently associated with in-hospital and 30-day death. Conclusions: High hs-CRP levels were not associated with impaired myocardial perfusion score. Microcirculatory impairment may be related to an increased inflammatory process, independent from high hs-CRP levels

Cerebral Embolic Protection during Transcatheter Aortic-Valve Replacement.

BACKGROUND: Transcatheter aortic-valve replacement (TAVR) for the treatment of aortic stenosis can lead to embolization of debris. Capture of debris by devices that provide cerebral embolic protection (CEP) may reduce the risk of stroke. METHODS: We randomly assigned patients with aortic stenosis in a 1:1 ratio to undergo transfemoral TAVR with CEP (CEP group) or without CEP (control group). The primary end point was stroke within 72 hours after TAVR or before discharge (whichever came first) in the intention-to-treat population. Disabling stroke, death, transient ischemic attack, delirium, major or minor vascular complications at the CEP access site, and acute kidney injury were also assessed. A neurology professional examined all the patients at baseline and after TAVR. RESULTS: A total of 3000 patients across North America, Europe, and Australia underwent randomization; 1501 were assigned to the CEP group and 1499 to the control group. A CEP device was successfully deployed in 1406 of the 1489 patients (94.4%) in whom an attempt was made. The incidence of stroke within 72 hours after TAVR or before discharge did not differ significantly between the CEP group and the control group (2.3% vs. 2.9%; difference, -0.6 percentage points; 95% confidence interval, -1.7 to 0.5; P = 0.30). Disabling stroke occurred in 0.5% of the patients in the CEP group and in 1.3% of those in the control group. There were no substantial differences between the CEP group and the control group in the percentage of patients who died (0.5% vs. 0.3%); had a stroke, a transient ischemic attack, or delirium (3.1% vs. 3.7%); or had acute kidney injury (0.5% vs. 0.5%). One patient (0.1%) had a vascular complication at the CEP access site. CONCLUSIONS: Among patients with aortic stenosis undergoing transfemoral TAVR, the use of CEP did not have a significant effect on the incidence of periprocedural stroke, but on the basis of the 95% confidence interval around this outcome, the results may not rule out a benefit of CEP during TAVR. (Funded by Boston Scientific; PROTECTED TAVR ClinicalTrials.gov number, NCT04149535.)