L-arginine and Its Derivatives Correlate with Exercise Capacity in Patients with Advanced Heart Failure.

Methylated arginine metabolites interrupt nitric oxide synthesis, which can result in endothelium dysfunction and inadequate vasodilation. Since little is known about the dynamics of arginine derivatives in patients with heart failure (HF) during physical exercise, we aimed to determine this as well as its impact on the patient outcomes. Fifty-one patients with HF (left ventricle ejection fraction-LVEF ≤ 35%, mean 21.7 ± 5.4%) underwent the cardiopulmonary exercise test (CPET). Plasma concentrations of L-arginine, citrulline, ornithine, asymmetric dimethylarginine (ADMA), and symmetric dimethylarginine (SDMA) were measured before and directly after CPET. All patients were followed for a mean of 23.5 ± 12.6 months. The combined endpoint was: any death, urgent heart transplantation, or urgent LVAD implantation. L-arginine concentrations increased significantly after CPET (p = 0.02), when ADMA (p = 0.01) and SDMA (p = 0.0005) decreased. The parameters of better exercise capacity were positively correlated with post-CPET concentration of L-arginine and inversely with post-CPET changes in ADMA, SDMA, and baseline and post-CPET SDMA concentrations. Baseline and post-CPET SDMA concentrations increased the risk of endpoint occurrence (HR 1.02, 95% CI 1.009-1.03, p = 0.04 and HR 1.02, 95% CI 1.01-1.03, p = 0.02, respectively). In conclusion, in patients with HF, extensive exercise is accompanied by changes in arginine derivatives that can reflect endothelium function. These observations may contribute to the explanation of the pathophysiology of exercise intolerance in HF.

Conservative treatment as a therapeutic option for penetrating aortic ulcer of the aortic arch in a patient with bicuspid aortic valve.

Penetrating aortic ulcer (PAU) is ulceration of an aortic atherosclerotic plaque penetrating through the internal lamina into the media. PAU is a rare condition and occurs in 2% - 7% of acute aortic syndromes (AAS); however, the actual incidence is unknown because of asymptomatic patients. One may treat it conservatively as well as surgically. We present a case of a 54-year-old man, who was admitted to hospital due to the exaggeration of exertional chest pain and persistent headaches. During coronary angiography, the suspicion of PAU was raised. Contrast-enhanced computed tomography confirmed the diagnosis. Transesophageal echocardiography showed bicuspid aortic valve with minimal calcification, the dilated ascending aorta, large atherosclerotic plaques in the aortic arch with ulceration (thickness: 5.0 - 5.5mm, diameter: 5 - 6 mm, depth: 3 - 4 mm), without intramural hematoma. Conservative treatment was chosen with uneventful 2-year follow-up. Although surgical management is advocated for patients with PAU type A, we demonstrated that type A PAU can be successfully treated conservatively as well.

Viral Heart Disease and Acute Coronary Syndromes - Often or Rare Coexistence?

BACKGROUND: Clinical presentation of viral myocarditis can mimic acute coronary syndrome and making diagnosis of viral heart disease (VHD) may be challenging. The presence of coronary artery disease (CAD) does not always exclude VHD and these entities can coexist. However, the incidence of co-occurrence of CAD and VHD is not precisely known. Moreover, inflammatory process caused by viruses may result in atherosclerotic plaque destabilization. METHODS: The goal of this work is to summarize the current knowledge about co-occurrence of VHD and CAD. This article presents the importance of inflammatory process in both diseases and helps to understand pathophysiological mechanisms underlying their coexistence. It provides information about making differential diagnosis between these entities, including clinical presentation, noninvasive imaging features and findings in endomyocardial biopsy. Although currently there are no standard therapy strategies in coexistence of VHD and CAD, we present some remarkable aspects of treatment of patients, in whom VHD co-occurs with CAD. RESULTS: Viral heart disease may occur both in patients without and with atherosclerotic plaques in coronary arteries. Destabilization of atherosclerotic plaques in coronary arteries can be facilitated by inflammatory process. Increased inflammatory infiltrates in the coronary lesions of patients with VHD can lead to plaques' instability and consequently trigger acute coronary syndrome. CONCLUSION: In this article we attempted to present that co-occurrence of VHD and CAD may have therapeutic implications and as specific antiviral treatment is currently available, proper diagnosis and treatment can improve patient's condition and prognosis.