Heart rate-dependent mitral regurgitation.

Mitral regurgitation (MR) is a particularly dynamic valvular disorder. Extreme bradycardia can lead to prolonged left ventricular filling time and mitral annular dilatation, hence causing secondary MR in a structurally normal mitral valve.

Normal procalcitonin, C-reactive protein, and negative blood cultures in infective endocarditis with a massive residual vegetation: a case report.

BACKGROUND: Infective endocarditis (IE) is a serious infection with high morbidity and mortality that involves the endocardial lining of the heart. Most cases of IE are due to bacteria although other atypical micro-organisms can also be involved. Procalcitonin (PCT) is a biomarker that is used in the diagnosis of bacterial infections. CASE SUMMARY: We present the case of a 54-year-old patient with bacterial endocarditis who has been regularly visiting his cardiologist for follow-up on a mitral valve prolapse and moderate mitral regurgitation (MR) for the last 11 years. During his last visit, transthoracic echocardiography (TTE) showed a previously non-existent structure on the posterior mitral valve leaflet with severe MR. Blood cultures were positive for Streptococcus viridans. On admission, he had elevated levels of PCT and C-reactive protein which returned to normal values after 4 weeks of intravenous antibiotic therapy. His follow-up blood cultures, taken after normalization of PCT, did not show bacterial growth; however, on TTE he had severe mitral regurgitation and a persistent vegetation which had slightly increased in size after completion of the full antibiotic course. He was referred for mitral valve replacement surgery. DISCUSSION: Normalization of procalcitonin levels may correlate with negative blood cultures in cases of IE with residual vegetations. The optimal time for surgery in such patients is difficult to define but even in circumstances with less infective organisms such as S. viridans and late in the course of the disease residual vegetations remain a serious risk factor for embolic events. Randomized controlled clinical trials are needed in order to have better recommendations with solid evidence regarding prophylaxis and treatment in IE.

Efficacy and safety of intensified antiplatelet therapy on the basis of platelet reactivity testing in patients after percutaneous coronary intervention: systematic review and meta-analysis.

BACKGROUND: ADP-specific platelet function assays were shown to predict thrombotic events, and might be helpful to select candidates for more potent antiplatelet therapy. We aimed to determine the efficacy and safety of giving intensified antiplatelet therapy on the basis of platelet reactivity testing for patients undergoing percutaneous coronary intervention (PCI). METHODS: Electronic databases were searched to find prospective, randomized trials that reported the clinical impact of using an intensified antiplatelet protocol (repeated loading or elevated maintenance doses of clopidogrel, prasugrel or glycoprotein IIb/IIIa inhibitor) on the basis of ADP-specific platelet reactivity testing (VerifyNow, Multiplate, VASP or light transmission aggregometry) compared to standard-dose clopidogrel. Evaluated efficacy measures included cardiovascular death, non-fatal myocardial infarction and definite/probable stent thrombosis (ST), while major bleeding events were recorded as safety endpoint. RESULTS: Between 2008 and 2011, 10 clinical trials comprising 4213 randomized patients were identified. Compared to standard antiplatelet therapy, the intensified protocol was associated with a significant reduction in cardiovascular mortality, ST and myocardial infarction (p<0.01 for all). There was no difference in the rate of major bleeding events between intensified and standard groups (p=0.44). Although the observed effects regarding mortality, ST and bleeding were not heterogeneous, meta-regression analysis revealed that the net clinical benefit of the intensified treatment significantly depended on the risk of ST with standard-dose clopidogrel (p=0.023). CONCLUSION: Intensifying antiplatelet therapy on the basis of platelet reactivity testing reduces cardiovascular mortality and ST after PCI; however, the net benefit of this approach depends on the risk of ST with standard-dose clopidogrel.

Permanent pacing in patients with recurrence of symptoms and relapse of left ventricular obstruction at midcavity level after alcohol septal ablation.

Treatment of symptom recurrence after initially successful alcohol septal ablation (ASA) in hypertrophic obstructive cardiomyopathy (HOCM) when accompanied by relapse of intracavitary left ventricular pressure gradient (LVG) is guided by the underlying mechanism. We describe our experience with permanent pacing in three patients with relapse of both LVG and symptoms 7 to 12 months after successful ASA. Even though pressure gradient recurrence was observed at midventricular level, we were able to achieve symptomatic improvement and LVG reduction after right ventricular apex pacing in all three cases. The effect on symptoms was long lasting-the 6-month followup echo-stress tests confirmed good exercise capacity and lack of provocable LVG. We found pacing to be a safe and effective treatment option in this clinical scenario. Based on our overall observations, we propose pacing as a niche treatment for patients with recurrence of LVG at midventricular level after ASA.

Tailoring clopidogrel dose according to multiple electrode aggregometry decreases the rate of ischemic complications after percutaneous coronary intervention.

Multiple studies have shown a correlation between high on-treatment platelet reactivity (HPR) and ischemic complications after percutaneous coronary interventions (PCI); however, the role of platelet reactivity testing in order to adjust clopidogrel dose is debated. We sought to determine whether a strategy incorporating platelet reactivity testing with the Multiplate analyzer to tailor the dose of clopidogrel is superior to standard clopidogrel treatment after PCI. Between May 2008 and June 2009, 192 consecutive patients undergoing PCI were randomized to a tailored treatment strategy using the Multiplate analyzer or to uniform administration of 75 mg clopidogrel. In the tailored group, platelet function was assessed 24 h after clopidogrel loading, and patients with HPR (>46 U) received an additional 600 mg loading dose and 150 mg clopidogrel thereafter for one month. The primary endpoint was the composite of cardiac death, myocardial infarction, ischemic stroke or definite/probable stent thrombosis during six months. In the tailored group, a repeated loading dose of 600 mg clopidogrel significantly decreased platelet reactivity in patients with HPR (61.0 U [IQR: 52.5-71.5] vs. 21.5 U [15.8-30.5]; P < 0.0001) that remained unchanged during the maintenance phase on 150 mg clopidogrel (25.0 U [IQR: 19.8-27.0]; P = 0.20). The incidence of the primary endpoint was significantly higher in the standard clopidogrel group as compared to the Multiplate-tailored arm (5.3% vs. 0%, P = 0.03). In parallel, MACCE-free survival significantly improved in patients with Multiplate-tailored therapy (Kaplan-Meier log-rank: P = 0.02). Increasing the dose of clopidogrel according to the Multiplate assay may reduce ischemic complications in patients on clopidogrel after PCI.