Cardio-microcurrent device for chronic heart failure: first-in-human clinical study.

AIMS: Most devices for treating ambulatory Class II and III heart failure are linked to electrical pulses. However, a steady electric potential gradient is also necessary for appropriate myocardial performance and may be disturbed by structural heart diseases. We investigated whether chronic application of electrical microcurrent to the heart is feasible and safe and improves cardiac performance. The results of this study should provide guidance for the design of a two-arm, randomized, controlled Phase II trial. METHODS AND RESULTS: This single-arm, non-randomized pilot study involved 10 patients (9 men; mean age, 62 ± 12 years) at two sites with 6 month follow-up. All patients had New York Heart Association (NYHA) Class III heart failure and non-ischaemic dilated cardiomyopathy, with left ventricular ejection fraction (LVEF) <35%. A device was surgically placed to deliver a constant microcurrent to the heart. The following tests were performed at baseline, at hospital discharge, and at six time points during follow-up: determination of LVEF and left ventricular end-diastolic/end-systolic diameter by echocardiography; the 6 min walk test; and assessment of NYHA classification and quality of life (36-Item Short-Form Health Survey questionnaire). Microcurrent application was feasible and safe; no device-related or treatment-related adverse events occurred. During follow-up, rapid and significant signal of efficacy (P < 0.005) was present with improvements in LVEF, left ventricular end-diastolic diameter, left ventricular end-systolic diameter, and distance walked. For eight patients, NYHA classification improved from Class III to Class I (for seven, as early as 14 days post-operatively); for one, to Class II; and for one, to Class II/III. 36-Item Short-Form Health Survey questionnaire scores also improved highly significantly. CONCLUSIONS: Chronic application of microcurrent to the heart is feasible and safe and leads to a rapid and lasting improvement in heart function and a near normalization of heart size within days. The NYHA classification and quality of life improve just as rapidly.

Contractile reserve assessed by dobutamine test identifies super-responders to cardiac resynchronization therapy.

INTRODUCTION: In this study, we sought to determine whether myocardial contractile reserve (CR) assessed by dobutamine stress echocardiography (DSE) can identify patients who experience nearly complete normalization of left ventricular (LV) function after the implantation of a cardiac resynchronization therapy (CRT) pacemaker. MATERIAL AND METHODS: The study group consisted of 55 consecutive patients with non-ischemic dilated cardiomyopathy, LV ejection fraction (LVEF) < 35%, and prolonged QRS complex duration, who were scheduled for CRT pacemaker implantation. The DSE (20 µg/kg/min) was performed in all patients. The CR assessment was based on a change in the wall motion score index (ΔWMSI) and ΔLVEF during DSE. Super-response was defined as an increase in LVEF to > 50% and reduction in left ventricular end-systolic dimension to < 40 mm 12 months following the CRT implantation. RESULTS: A total of 7 patients (12.7%) were identified as super-responders to CRT. When compared to non-super-responders, these patients had significantly higher values of the dobutamine-induced change in ΔWMSI (1.031 ±0.120 vs. 0.49 ±0.371, p < 0.01), and ΔEF (17.9 ±2.2 vs. 8.8 ±6.2, p < 0.01). Receiver operating characteristic analysis showed that dobutamine-induced changes in ΔWMSI ≥ 0.7 and ≥ 14% for ΔEF are the best discriminators for a super-response. Patients with ΔWMSI ≥ 0.7 and ΔEF ≥ 14% are significantly less often hospitalized (p < 0.01) for worsening of heart failure during 28.5 ±3.0 months of the follow-up. CONCLUSIONS: Contractile reserve assessed by DSE can identify patients with dilated cardiomyopathy who are likely to experience near normalization of LV function following CRT.

A misinterpretation of the left ventricular non-compaction-adult patient with primary pulmonary hypertension.

Non-compaction of the left ventricle is a rare cardiac malformation, defined as a primary cardiomyopathy caused by genetic malformations. Although the pathogenesis of this cardiomyopathy is unknown, there are two possible hypotheses (congenital and acquired) which lead to arrest in intrauterine endomyocardial morphogenesis. We are presenting a case of a 60-year-old woman, with a history of bradyarrhythmia, syncope and cyanosis. Two-dimensional echocardiography showed the thickened myocardium with prominent trabeculations and deep intertrabecular recesses in the two thirds of the apical part of left ventricle walls. The right side cavity was enlarged with hypertrophied wall. Tricuspid regurgitation was moderate. Systolic pressure in the right ventricle was 70mmHg. Catheterization of the right heart showed high pressure in the pulmonary artery. According to publications, this is a very rare case with the presence of possible primary pulmonary hypertension and non-compaction of the left ventricle.

[Implantable cardioverter-defibrillator oversensing due to electric shock].

INTRODUCTION: We described the first case of oversensing due to electric shock in Serbia, in a 54-year-old man who had implantable cardioverter-defibrillator (ICD). CASE OUTLINE: In July 2002, the patient had acute anteroseptal myocardial infarction and ventricular fibrillation (VF) which was terminated with six defibrillation shocks of 360 J. Coronary angiography revealed 30% stenosis of circumflex artery, the left anterior descending coronary artery was recanalized and the right coronary artery was without stenosis. Left ventricular ejection fraction was 20%. In December 2003, an electrophysiology study was performed and ventricular tachycardia (VT) was induced and terminated with 200 J defibrillation shock. Single chamber ICD Medtronic Gem III VR was implanted in January 2004 and defibrillation threshold was 12 J. The patient was followed up during three years every three months and there were no VT/VF episodes and VT/VF therapies. In December 2007, the patient experienced electric shock through the fork while he was making barbecue on the electric grill. ICD recognized this event in VF zone (oversensing) and delivered defibrillation shock of 18 J. The electrogram of the episode showed ventricular sensing--intrinsic sinus rhythm with electric shock potentials which were misidentified as VF. After charge time of 3.16 seconds, ICD delivered defibrillation shock and sinus rhythm was still present. CONCLUSION: Oversensing of ICD has different aetiology and the most common cause is supraventricular tachyarrhythmia.

[Brugada syndrome--a brand new case].

BACKGROUND: Brugada syndrome (BS) is a disorder characterized by syncope or sudden death associated with one of several electrocardiographic (ECG) patterns characterized by incomplete right bundle branch block and ST elevation in the anterior precordial leads. Patients with BS are prone to develop ventricular tachyarrhythmias that may lead to syncope, cardiac arrest, or sudden cardiac death. CASE REPORT: A 58-year-old woman is the first described case of Brugada syndrome in Serbia with intermittent typical changes in basic electrocardiography (ECG): ST segment elevation in the precordial chest leads like dome or coved--major form or type I. For the last 27 years the patient had suffered of palpitations and dizziness, without syncopal events. Her sister had died suddenly during the night in sleep. During 24-hour Holter monitoring the patient had ventricular premature beats during the night with R/T phenomenon and during the recovery phase of exercise testing had rare premature ventricular beats as the consequence of parasympatethic stimulation. Late potentials were positive. Echocardiography revealed left ventricular ejection fraction of 60%. We performed coronary angiography and epicardial coronary arteries were without significant stenosis and structural heart disease was excluded. In the bigining of the electrophysiological study ECG was normal, and after administration of Propaphenon i.v. Brugada syndrome unmasked with appearance of type I ECG pattern. A programed ventricular stimulation induced non sustained ventricular tachycardia. One-chamber implantable cardioverter defibrillator was implanted and the patient was treated with a combination od amiodarone and metoprolol per os. After one-year folow-up, there were no episodes of ventricular tachycardia and ventricular fibrillation. CONCLUSION: Brugada syndrome is a myocardial disorder which prognosis and therapy are related to presence of ventricular fibrillation or ventricular tachycardia. Electrophysiologicaly induced malignant ventricular disorders class I are indication for implantation of cardioverter defibrilator, as also occurred in presented patient.