Eustachian valve endocarditis (EVE) is a distinctly rare and underdiagnosed entity. We report 2 new cases caused by vancomycin resistant Staphylococcus aureus and Staphylococcus hominis diagnosed on transesophageal echocardiography (TEE). Although, 63% of Eustachian valve endocarditis is caused by Staphylococcus aureus, we report the first case of vancomycin resistant Staphylococcus aureus and first case related to implantable venous access systems. EVE is now seen more commonly in elderly population with diverse microbial cultures and antibiotic sensitivities. TTE is the first modality for investigation of EVE, however a negative TTE does not preclude the diagnosis, as only 88% of cases were diagnosed on TEE.

Myocardial fibrosis, a major pathophysiologic substrate of heart failure with preserved ejection fraction (HFPEF), is modulated by multiple pathways including the renin-angiotensin system. Direct renin inhibition is a promising anti-fibrotic therapy since it attenuates the pro-fibrotic effects of renin in addition to that of other effectors of the renin-angiotensin cascade. Here we show that the oral renin inhibitor aliskiren has direct effects on collagen metabolism in cardiac fibroblasts and prevented myocardial collagen deposition in a non-hypertrophic mouse model of myocardial fibrosis. Adult mice were fed hyperhomocysteinemia-inducing diet to induce myocardial fibrosis and treated concomitantly with either vehicle or aliskiren for 12 weeks. Blood pressure and plasma angiotensin II levels were normal in control and hyperhomocysteinemic mice and reduced to levels lower than observed in the control group in the groups treated with aliskiren. Homocysteine-induced myocardial matrix gene expression and fibrosis were also prevented by aliskiren. In vitro studies using adult rat cardiac fibroblasts also showed that aliskiren attenuated the pro-fibrotic pattern of matrix gene and protein expression induced by D,L, homocysteine. Both in vivo and in vitro studies demonstrated that the Akt pathway was activated by homocysteine, and that treatment with aliskiren attenuated Akt activation. In conclusion, aliskiren as mono-therapy has potent and direct effects on myocardial matrix turnover and beneficial effects on diastolic function.

Rhabdomyolysis is an uncommon but life-threatening adverse effect of simvastatin therapy. A 73-year-old male on chronic simvastatin therapy received azithromycin for acute bronchitis. He presented with weakness of all extremities with a significant increase in creatinine phosphokinase levels and acute kidney injury. Simvastatin was stopped and supportive therapy with intravenous saline and bicarbonate was initiated. The serum creatinine and creatine phosphokinase returned to baseline in the next 7 days. Two months later, simvastatin was resumed without any recurrence of symptoms. Our case report highlights the rare description of rhabdomyolysis caused by a drug interaction between simvastatin with azithromycin.

Inhibition of the renin angiotensin system has beneficial effects in cardiovascular prevention and treatment. The advent of orally active direct renin inhibitors adds a novel approach to antagonism of the renin-angiotensin system. Inhibition of the first and rate-limiting step of the renin angiotensin cascade offers theoretical advantages over downstream blockade. However, the recent discovery of the (pro)renin receptor which binds both renin and prorenin, and which can not only augment catalytic activity of both renin and prorenin in converting angiotensinogen to angiotensin I, but also signal intracellularly via various pathways to modulate gene expression, adds a significant level of complexity to the field. In this review, we will examine the basic and clinical data on renin and its inhibition in the context of cardiovascular pathophysiology.

This small, single-center randomized study found that among carefully selected peripheral arterial interventions, SD may be feasible and safe. However, patient satisfaction and perceived safety were significantly lower among SD compared to the OS condition. Larger prospective studies are warranted to confirm these findings.