Renata Okrajsek

Atorvastatin Therapy May Reduce the Incidence of Sudden Cardiac Death in Patients With Advanced Chronic Heart Failure

BACKGROUND In retrospective studies, statin therapy has been related to decreased incidence of sudden cardiac death (SCD) in heart failure. We sought to prospectively investigate a relation between atorvastatin therapy and SCD in patients with advanced chronic heart failure. METHODS AND RESULTS We enrolled 110 patients with heart failure with a left ventricular ejection fraction less than 30% and cholesterol level greater than 150 mg/dL. Fifty-five patients were randomized to atorvastatin (10 mg/day) (statin group); the remaining 55 patients received no statins (controls). Patients were followed for 1 year. At baseline, the two groups did not differ in age, sex, left ventricular ejection fraction, cholesterol, B-type natriuretic peptide, heart rate variability, or QT variability. During follow-up, 29 patients died (26%) and 2 patients (2%) underwent heart transplantation. Of the 29 deaths, 13 were attributed to pump failure, 15 were attributed to SCD, and 1 was attributed to noncardiac causes. All-cause mortality was lower in the statin group (9/55, 16%) than in controls (20/55, 36%) (P = .017). The same was true of the SCD rate (3/55 [5%] vs. 12/55 [22%], P = .012), but not of the pump failure (5/55 [9%] vs. 8/55 [15%], P = .38). SCD-free survival was 2.3-times higher in the statin group than in controls (P = .01). CONCLUSIONS Atorvastatin therapy seems to be associated with decreased incidence of SCD in patients with advanced chronic heart failure. Larger studies are ongoing to confirm this hypothesis.

Relation of B-Type Natriuretic Peptide Level in Heart Failure to Sudden Cardiac Death in Patients With and Without QT Interval Prolongation

Increased levels of B-type natriuretic peptide (BNP) are associated with prolongation of the action potential in ventricular myocardium. We investigated the relation of a BNP increase, QT interval, and sudden cardiac death (SCD) in the presence of heart failure (HF). We enrolled 398 patients with HF, New York Heart Association class III or IV, and left ventricular ejection fraction <40%. At baseline and after 3 months, we measured BNP and the QT interval. A BNP increase was defined as a change in BNP of ≥+10%. The QTc interval was calculated using the Bazett formula. QTc interval prolongation was defined as a change in QTc of ≥+10%. The patients were followed up for 1 year. During a 3-month period, BNP increased significantly in 53% of the patients (group 1) and did not in 47% (group 2). During the same period, the QTc interval was more prolonged in group 1 (+44 ± 12 ms) than in group 2 (+7 ± 6 ms; p = 0.01). During 1 year of follow-up, 20 patients died suddenly (SCD), 16 from pump failure. Although the SCD rates did not differ between the 2 groups (5.7% in group 1 vs 4.2% in group 2, p = 0.53), they were significantly greater in the patients in group 1 with QTc interval prolongation ≥+10% (13.8%, p <0.001). The Kaplan-Meier-derived SCD-free survival rates were 2.9 times greater in patients without QTc interval prolongation than in those with prolonged QTc (p <0.001). QTc interval prolongation was an independent correlate of SCD (p = 0.006), but BNP increase was not (p = 0.32). In conclusion, a BNP increase in patients with HF was associated with an increased risk of SCD only in patients with QTc interval prolongation.

Heart transplantation due to advanced chronic heart failure after complete correction of tetralogy of Fallot.

A 52-year-old patient decades after complete correction of tetralogy of Fallot is presented. The main late complication was left ventricular failure with consequential congestive heart failure. Heart transplantation was the only therapeutic option.

POOR STEM CELL MOBILIZATION IN PATIENTS WITH ADVANCED CHRONIC HEART FAILURE IS ASSOCIATED WITH INCREASED RED CELL DISTRIBUTION WIDTH

patient’s blood, they do not effectively destroy the plasma cells that produce the DSA. Bortezomib, a proteasome inhibitor, leads to cellcycle arrest and apoptosis of plasma cells. Our hypothesis was to determine if Bortezomib added to a regimen of intravenous immunoglobulin (IVIG) and plasmapheresis resulted in prolonged reduction of DSA in a non-compliant, teenage heart transplant patient with humoral rejection. Methods and Materials: The regimen used at our institution for humoral rejection consisted of plasmapheresis and IVIG every other day for two weeks. Bortezomib was administered at a dose of 1.3 mg/m2 on day one, four, eight, and eleven of the treatment cycle per our institutional protocol with all the appropriate premedications. The patient received two rounds of treatment with plasmapheresis, IVIG, and Bortezomib initiated on Day 1 and Day 96. Panel Reactive Antibody tests were performed using a Luminex microsphere and antibody levels were measured by using median fluorescence intensity (MFI). Results: The trend in the strength of DSA in the patient is shown in Figure 1.