Research of predictive factors for cardiac resynchronization therapy: a prospective study comparing data from phase-analysis of gated myocardial perfusion single-photon computed tomography and echocardiography : Trying to anticipate response to CRT.

BACKGROUND: Cardiac resynchronization therapy (CRT) reduces morbidity and mortality in chronic systolic heart failure. About 20% of implanted patients are considered as "non-responders". This study aimed to evaluate gated myocardial perfusion single-photon emission computed tomography (GMPS) phase parameters as compared to echocardiography in the assessment of predictors for response to CRT before and after CRT activation. METHODS: Forty-two patients were prospectively included during 15 months. A single injection of 99mTc-tetrofosmin was used to acquire GMPS phase pre- and post-CRT activation. Indicators of positive CRT response were improvement of functional status and 15% reduction in left ventricular end-systolic volume at 3 months. RESULTS: Phase parameters at baseline were similar in the two groups with no influence of perfusion data. Phase parameters after CRT activation were significantly improved in the responders' group (Δ Bandwidth -19° ± 24° vs. 13° ± 31°, p = 0.001; Δ SD -20° ± 30° vs. 26° ± 46°, p = 0.001; Δ Entropy -11 ± 12 vs. 2 ± 6%, p = 0.001). Feasibility and reproducibility were higher for GMPS. CONCLUSION: Acute phase modifications after CRT activation may predict response to CRT immediately after implantation, but not at baseline, even when adjusted to perfusion data.

Should furosemide be avoided in acute right ventricular myocardial infarction?

BACKGROUND: Diuretics are conventionally prohibited in acute right ventricular myocardial infarction. AIMS: To assess the benefit of diuretics compared to fluid expansion in patients with inferior myocardial infarction extended to the right ventricule. METHODS: Of 295 patients admitted for inferior or posterior acute myocardial infarction between November 2008 and November 2010, 77 had a right ventricular extension. Among these 77 patients, 19 presented with oligoanuria (<0.5 mL/kg per hour) and no criteria for cardiogenic shock. Overall, 11 patients were treated by low dose of furosemide (40 to 80 mg) and eight received fluid expansion using isotonic saline solution. RESULTS: Baseline right ventricular dilatation and dysfunction, systolic blood pressure and heart rate were similar between the groups. Twenty-four hours after treatment, urine output was similar between the two groups but only the patients in the diuretic group improved their blood pressure (103 ± 16 mmHg versus 127 ± 20 mmHg, P < 0.001), heart rate (71 ± 15 bpm versus 76 ± 13 bpm, P = 0.03), creatinin level and alanine aminotrasferase plasmatic level. Hospitalization duration and the need of inotropic support were similar in the two groups. CONCLUSIONS: Diuretics and fluid expansion provide similar efficiency for triggering diuresis in patients with right ventricular infarction and oligoanuria but only diuretics seem to be associated with improvement in hemodynamic status and venous congestion.

Role of serotonin 5-HT2A receptors in the development of cardiac hypertrophy in response to aortic constriction in mice.

Serotonin, in addition to its fundamental role as a neurotransmitter, plays a critical role in the cardiovascular system, where it is thought to be involved in the development of cardiac hypertrophy and failure. Indeed, we recently found that mice with deletion of monoamine oxidase A had enhanced levels of blood and cardiac 5-HT, which contributed to exacerbation of hypertrophy in a model of experimental pressure overload. 5-HT2A receptors are expressed in the heart and mediate a hypertrophic response to 5-HT in cardiac cells. However, their role in cardiac remodeling in vivo and the signaling pathways associated are not well understood. In the present study, we evaluated the effect of a selective 5-HT2A receptor antagonist, M100907, on the development of cardiac hypertrophy induced by transverse aortic constriction (TAC). Cardiac 5-HT2A receptor expression was transiently increased after TAC, and was recapitulated in cardiomyocytes, as observed with 5-HT2A in situ labeling by immunohistochemistry. Selective blockade of 5-HT2A receptors prevented the development of cardiac hypertrophy, as measured by echocardiography, cardiomyocyte area and heart weight-to-body weight ratio. Interestingly, activation of calmodulin kinase (CamKII), which is a core mechanism in cardiac hypertrophy, was reduced in cardiac samples from M100907-treated TAC mice compared to vehicle-treated mice. In addition, phosphorylation of histone deacetylase 4 (HDAC4), a downstream partner of CamKII was significantly diminished in M100907-treated TAC mice. Thus, our results show that selective blockade of 5-HT2A receptors has beneficial effect in the development of cardiac hypertrophy through inhibition of the CamKII/HDAC4 pathway.