[Immunoadsorption in a patient with dilated cardiomyopathy. The first case in Hungary]. / Dilatatív cardiomyopathia immunadszorpciós kezelése. Az elso magyarországi eset kapcsán.

Dilated cardiomyopathy is the main cause of heart transplantation. The etiology is unknown in almost half of the cases. Many cardiac specific antibodies have been identified till now which can cause decreased cardiac function, ventricular tachycardia or sudden heart death. The prognosis of DCM is poor despite the development of medical treatment. Immunoadsorption is hopeful since, with the removal of antibodies, cardiac function and NYHA class can improve and LVAD/heart transplantation-free survival can be prolonged. At the University of Debrecen, Faculty of Medicine, Department of Internal Medicine, Division of Angiology, Intensive Care and Therapeutic Apheresis Unit we performed the first immunoadsorption. Our patient was a 43-year-old man with idiopathic dilated cardiomyopathy, NYHA class IV, a heart transplantation candidate, whose cardiac specific antibody, type IgG was indentified by Western blot. Before the treatment he had ejection fraction of 18%. Discussing with his cardiologists we decided for immunoadsorption therapy. We performed 5 cycles on consecutive days in Intensive Care Unit. After 1 month we detected improvement in exercise capacity. We detected improvement in isovolemic contraction (from 465 mmHg/s to 575 mmHg/s), increased stroke volume (from 49 ml to 66 ml). After 3 months we repeated SPECT investigation which showed improvement in ejection fraction, from 18% to 32%. Orv Hetil. 2018; 159(13): 532-536.

Circulating ACE2 activity correlates with cardiovascular disease development.

It was shown recently that angiotensin-converting enzyme activity is limited by endogenous inhibition in vivo, highlighting the importance of angiotensin II (ACE2) elimination. The potential contribution of the ACE2 to cardiovascular disease progression was addressed. Serum ACE2 activities were measured in different clinical states (healthy, n=45; hypertensive, n=239; heart failure (HF) with reduced ejection fraction (HFrEF) n=141 and HF with preserved ejection fraction (HFpEF) n=47). ACE2 activity was significantly higher in hypertensive patients (24.8±0.8 U/ml) than that in healthy volunteers (16.2±0.8 U/ml, p=0.01). ACE2 activity further increased in HFrEF patients (43.9±2.1 U/ml, p=0.001) but not in HFpEF patients (24.6±1.9 U/ml) when compared with hypertensive patients. Serum ACE2 activity negatively correlated with left ventricular systolic function in HFrEF, but not in hypertensive, HFpEF or healthy populations. Serum ACE2 activity had a fair diagnostic value to differentiate HFpEF from HFrEF patients in this study. Serum ACE2 activity correlates with cardiovascular disease development: it increases when hypertension develops and further increases when the cardiovascular disease further progresses to systolic dysfunction, suggesting that ACE2 metabolism plays a role in these processes. In contrast, serum ACE2 activity does not change when hypertension progresses to HFpEF, suggesting a different pathomechanism for HFpEF, and proposing a biomarker-based identification of these HF forms.

The effect of sleep apnea on QT interval, QT dispersion, and arrhythmias.

BACKGROUND: QT interval (QT) and QT dispersion (QTd) are electrocardiograph (ECG) parameters for the evaluation of myocardial repolarization. The inhomogeneity of ventricular repolarization is associated with ventricular arrhythmias. An increased QT, QTd, and increased incidence of nocturnal cardiac rhythm disturbances have been described in patients with obstructive sleep apnea (OSA), while other investigators did not find a relationship between ventricular arrhythmias and OSA. HYPOTHESIS: The aim of this study was to examine the occurrence of ventricular arrhythmias and to measure QT parameters in patients with untreated OSA using an ambulatory Holter-ECG. METHODS: A total of 25 patients with untreated OSA were studied. After routine biochemical investigation and 2-dimensional, M-mode echocardiography, a 24-hour Holter-ECG was recorded to detect cardiac arrhythmias and QT parameters. QT parameters were measured by the QT Guard system. RESULTS: Only the QT interval increased significantly during the nighttime period (nocturnal QT interval: 423.1 +/- 34.6 ms, daytime QT interval: 381.6 +/- 33.8 ms, 24-hour QT interval: 394.7 +/- 31.1 ms). However, during the nighttime QT interval (422.8 +/- 14.9 ms), QTd (31.2 +/- 11.0 ms) and QT dispersion (30.5 +/- 10.2 ms) did not show any change compared to 24-hour (QTc interval: 423.7 +/- 14.2 ms, QTd: 28.8 +/- 9.4 ms, QTcd: 30.5 +/- 9.43 ms) and daytime levels (QTc interval: 423.9 +/- 14.3 ms, QTd: 27.3 +/- 10.7 ms, QTcd: 29.9 +/- 11.1 ms). None of the patients had ventricular arrhythmias. CONCLUSIONS: QTd and QTcd did not increase during the nighttime period. Our study did not show an increased risk of ventricular arrhythmias in this population during the monitoring period.

[Arrhythmias in patients with obstructive sleep apnea]. / Szívritmuszavarok obstruktív alvási apnoéban.

The authors summarize the current knowledge on the types, prevalence, reasons, diagnosis and current therapy of arrhythmias occurring in patients with obstructive sleep apnea. Most of the patients with obstructive sleep apnea have nocturnal bradycardia (5-50%), paroxysmal tachyarrhythmia (atrial 35%; ventricular 0-15%), or both. The frequency of rhythm disturbances associated with the severity of the sleeping disorder. It is important to recognize the factors predisposing to arrhythmias and the early appropriate therapy of patients is essential, in order to protect patients from life threatening arrhythmias which may worsen the clinical outcome.