Perioperative erythropoietin protects the CNS against ischemic lesions in patients after open heart surgery.

AIM: The aim of this study was to establish erythropoietin as a protective factor against brain ischemia during open heart surgery. METHODS: A total of 36 consecutive patients scheduled for revascularization heart surgery were included in the study. Of the patients 18 received 3 intravenous doses of recombinant human erythropoietin (rHuEpo, 24,000 IU) and 18 patients received a placebo. Magnetic resonance imaging (MRI) to detect new brain ischemic lesions was performed. Additionally, S100A, S100B, neuron-specific enolase A and B (NSE-A and B) and the concentration of antibodies against N­methyl-D-aspartate receptors (NMDAR) to identify new neurological complications were determined. RESULTS: Patients who received rHuEpo showed no postoperative ischemic changes in the brain on MRI images. In the control group 5 (27.8 %) new ischemic lesions were found. The NMDAR antibody concentration, S100A, S100B and NSE showed no significant differences between the groups for new cerebral ischemia. High levels of lactate before and after external aortic compression (p = 0.022 and p = 0.048, respectively) and duration of operation could predict new ischemic lesions (p = 0.009). CONCLUSIONS: The addition of rHuEpo reduced the formation of lesions detectable by MRI in the brain and could be used clinically as neuroprotection in cardiac surgery.

All-comer treatment with bioresorbable vascular scaffold.

BACKGROUND: Bioresorbable vascular scaffolds (BVS) could overcome drug-eluting stents (DES) drawbacks connected with their permanent presence in the vessel wall. Studies exploring the clinical use of BVS are limited to the patients presenting with noncomplex, short and stable lesions. There are no prospective and randomized studies available in all-comer patients. METHODS AND RESULTS: We analyzed 31 patients, who received at least one BVS (Absorb(™)) between September 1, 2012 and November 1, 2014. Median follow-up period was 424 days. In one (3.2%) patient, we performed a target vessel revascularization (TVR). The death rate was 6.5%. One (3.2%) patient, who received both BVS and a bare metal stent (BMS), died of an acute stent thrombosis 8 days after the initial procedure. One (3.2%) patient died of a non-cardiac death. We did not encounter any target lesion revascularization (TLR) or myocardial infarction (MI). The major adverse cardiac events (MACE) rate was 3.2%. CONCLUSIONS: Implantation of BVS is a safe treatment option. Lesions should be carefully selected and prepared before BVS implantation. We need more data about the safety of BVS and BMS overlapping.

Standardization of the apex beat in the full left lateral position and its diagnostic value in detecting left ventricular dilatation.

AIMS: The aims of this study were to determine the characteristics of the apex beat in the full left lateral position in healthy adults, and to assess its value in the diagnosis of left ventricular dilatation. METHODS AND RESULTS: 77 healthy adults and 27 patients with left ventricular dilatation were evaluated by history, physical examination, electrocardiography, apexcardiography and complete transthoracic echocardiographic examination. The location, size and quality of the apex beat were determined in the 90-degree left lateral position. A palpable apex beat, located in the 5th or 6th intercostal space, was recorded in 87% of the healthy adults. The lateral margin was palpated in a 3-cm-wide area from the left anterior axillary line (LAAL) towards the mid-clavicular line (MCL). The mean diameter and area were 2.5 +/- 0.5 cm and 5.0 +/- 2.5 cm2, respectively. In 51% the apex impulse intensity was of medium degree, in 25% weak and in 24% strong. It was palpable in all patients with left ventricular enlargement in the 5th, 6th or 7th intercostal space. The lateral margin was located in a 4.5-cm-wide area, 3.5 cm left from the LAAL to 1 cm right from it. The mean diameter and area were 5.0 +/- 1.0 cm and 20.0 +/- 7.0 cm2, repectively. The intensity was weak in 56% and medium degree in the rest. The diameter > or = 4.0 cm was sensitive (96%) and specific (96%) for the enlarged left ventricle. The location of the apex beat with the cut-off point in the LAAL was equally sensitive but less specific (63%) for left ventricular dilatation. CONCLUSIONS: Palpation of the apex beat in the full left lateral position is very suitable for detecting the left ventricular dilatation at bedside. The size of the apex beat appears to be a more reliable diagnostic sign of left ventricular dilatation than its location.

Electrophysiology of anterograde right-atrial and left-atrial inputs to the atrioventricular node in patients with atrioventricular nodal re-entrant tachycardia.

AIMS: To study anterograde atrioventricular (A-V) nodal electrophysiological properties through the right-atrial (Ri) and left-atrial inputs (Li) under the pharmacological autonomic blockade (AUB) in patients with slow-fast A-V nodal re-entrant tachycardia (AVNRT) and in controls. METHODS AND RESULTS: Twenty-nine patients with slow-fast AVNRT and 15 control subjects were included. Programmed stimulation with single extrastimulus was performed from the right atrial appendage to test the Ri, and from the posterolateral coronary sinus to test the Li. The AUB was induced with intravenous atropine (0.04 mg/kg) and metoprolol (0.15 mg/kg). The A-V nodal conduction times, refractoriness, discontinuous conduction (≥ 40 ms atrial-His interval 'jump'), and inducibility of AVNRT or reciprocating beats were compared. The A-V nodal conduction times were longer: (i) through the Ri than Li, (ii) in patients than controls, and (iii) in baseline than after AUB--at slow rates in both groups and at fast rates in patients through the right input only (P < 0.05-0.001). A significantly longer slow pathway effective refractory period was demonstrated through the Li than the Ri in patients in baseline (P < 0.05). The discontinuous conduction was demonstrated 94 times in 25 of 29 (83%) patients and 15 times in 6 of 15 (40%) controls (P < 0.01), and was most frequently encountered with the Ri testing. Likewise, inducibility was manifested most frequently with the Ri testing (P = 0.08), and decreased after AUB during this testing only (P = 0.05). CONCLUSION: The inherent magnitude of discordance of A-V nodal conduction velocity, refractoriness, and parasympathetic modulation between the Ri and Li to the A-V node may play a role in the aetiology of AVNRT.

Factors influencing pacemaker generator longevity: results from the complete automatic pacing threshold utilization recorded in the CAPTURE Trial.

OBJECTIVES: The CAPTURE study evaluated the accuracy of automated atrial and right ventricular (RV) threshold algorithms. BACKGROUND: Modern pacemakers include many added features designed to improve the ease of patient follow-up, as well as algorithms to reduce pacing outputs and/or reduce the atrial or ventricular pacing percentages, thus improving longevity. METHODS: Automated atrial and RV threshold measurements were assessed versus manual measurements at 6 months. The projected longevity was assessed and compared between subjects with the threshold-tracking feature On versus Off. In addition, the projected longevity effect of device features to reduce atrial pacing and reduce ventricular pacing, and device characteristics such as battery size and high impedance leads (> or =1,000 ohms), was investigated. RESULTS: Atrial and RV manual versus automatic measurements were equivalent in 683 of 691 subjects (98.8%) and 736 of 746 subjects (98.7%), respectively. Thresholds were stable with 99.6% of atrial and 99.2% of RV consecutive measurements within +/-0.25V. Algorithms for threshold tracking, reducing ventricular pacing, and reducing atrial pacing were associated with 0.8, 0.9, and 0.2 years projected longevity improvements. High impedance leads were associated with a 0.8-year projected longevity improvement. Approximately 2 years of longevity improvement was projected for a 1-cc increase in device size. CONCLUSIONS: The atrial and RV algorithms were accurate and reliable in all leads tested. Threshold tracking, reduced ventricular pacing, and high impedance leads result in increased device longevity. Battery capacity was the strongest determinant of increased projected longevity.

Treatment of inappropriate sinus tachycardia with ivabradine.

BACKGROUND: Inappropriate sinus tachycardia is most often treated with beta-blockers; in resistant cases, nonpharmacologic treatment has been attempted. Recent case reports have shown a favorable response to ivabradine in some patients. METHODS: A total of 13 patients (11 women, 2 men) aged from 27 to 66 years (mean 42 +/- 8) and having inappropriate sinus tachycardia were treated with ivabradine 15 mg per day. RESULTS: In 12 patients whose previous therapy could be discontinued or who did not have previous medication the mean daily heart rate decreased from 94.0 +/- 10.0 to 74.6 +/- 5.2 bpm (mean +/- SD) after ivabradine treatment. In 10 patients in whom we could reliably measure the highest and lowest daily heart rates, the highest rate decreased from 150.3 +/- 13.4 to 120.6 +/- 9.8 and the lowest from 66.7 +/- 9.6 to 54.8 +/- 6.9. All of the differences were statistically significant (P < 0.001). The percentage of heart rate reduction correlated with the initial heart rate (P < 0.005). The remaining patient, who had been treated with metoprolol 300 mg per day for more than 10 years and still had a resting heart rate of 106 bpm, switched to 15 mg of ivabradine daily without discontinuation of drug therapy. After this switch, a decrease of 4 bpm was noted in her mean daily heart rate. CONCLUSIONS: The results of our study show that patients with inappropriate sinus tachycardia can be successfully treated with ivabradine.

Atrial tachycardia with atypical Wenckebach atrioventricular block after slow pathway ablation.

A case of a patient with dual supraventricular tachycardias, atrioventricular nodal tachycardia, and atrial tachycardia is presented. The former was successfully ablated, whereas the latter was inducible after the ablation of the former, but without clinical importance during follow-up. However, this tachycardia showed interesting characteristics, including dual atrioventricular Wenckebach periodicity, presumably due to multiple slow pathways.

Transition of orthodromic tachycardia into atrioventricular nodal tachycardia during radiofrequency ablation of an accessory pathway.

We report a patient with Wolff-Parkinson-White syndrome, in whom orthodromic atrioventricular reciprocating tachycardia directly passed over to atrioventricular nodal re-entrant tachycardia during radiofrequency ablation of the accessory pathway. After the accessory pathway ablation, there were no tachycardia recurrences.

Ventricular tachycardia induced by abuse of ephedrine in a young healthy woman.

INTRODUCTION: Ephedrine or ephedra herbal products have occasionally been used to enhance sports performance and energy or to aid weight loss. The most serious side effects are those on cardiovascular function, including acute myocardial infarction, severe hypertension, myocarditis and lethal cardiac arrhythmias. CASE REPORT: A 19-year-old woman was taking ephedrine to enhance her sports performance. After 10 days of this medication she developed hemodynamically unstable ventricular tachycardia resistant to cardioversion and amiodarone treatment. She converted to sinus rhythm 60 hours later, presumably when the plasma ephedrine level had sufficiently decreased. In an electrophysiological study the ventricular tachycardia could be induced and successfully ablated. There were no recurrences during follow-up of more than a year. The use of ephedrine carries a risk of development of life-threatening arrhythmias. DISCUSSION: Ephedrine alone cannot be considered as the ultimate cause of tachycardia in our patient; however, it is highly probable that ephedrine triggered the tachycardic attack. The proarrhythmic effect most likely occurred because of underlying idiopathic left ventricular tachycardia. Although the patient could have developed her first attack of ventricular tachycardia at any time in her life, it is highly improbable that the attack following the ephedrine abuse was purely coincidental. CONCLUSION: Our experience with the reported patient shows that ephedrine alone, or in combination with substances that increase its effects on the cardiovascular system, may also trigger paroxysms of non-ischemic ventricular tachycardia. The use of ephedrine carries a risk of development of life-threatening arrhythmias and should be discouraged.

Retrospective analysis of mode survival, reliability of atrial sensing and incidence of atrial tachyarrhythmias in 307 single-lead VDD pacemaker patients.

AIMS: The aim of this retrospective analysis was to investigate VDD mode survival, development of atrial tachyarrhythmias (AT), and long-term atrial sensing performance of VDD pacing systems. METHODS AND RESULTS: We implanted single-lead VDD pacemakers in patients with isolated atrioventricular block and performed a retrospective analysis of 307 patients who had their devices implanted between May 1994 and September 2001. In 39 patients (12.7%), the pacing mode had to be reprogrammed to a single-chamber ventricular pacing mode, mostly due to permanent AT. In 16 of these patients, the atrial sensing safety margin was less than 150%. The atrial sensing safety margin was insufficient, i.e. less than 100% in only seven patients. Although only 12 (3.9%) of the patients had a history of paroxysmal AT at the time of pacemaker implantation, 200 (65%) patients presented with AT during follow-up. The mean AT burden at the last follow-up was 2.5%. CONCLUSION: These data illustrate that single-lead VDD pacemakers can be applied without serious complications in a highly selected group of patients. Our main concern is the development of AT in a large part of our population. Over a 10-year period, two thirds of our patients presented with AT.

Effects of systolic atrial function on plasma renin activity and natriuretic peptide secretion after high rate atrial and ventricular pacing in dogs.

Rapid atrial rates cause electrical, structural remodeling, and neuro-humoral changes. This study compares the effects of mechanical remodeling on plasma renin activity (PRA) and atrial natriuretic peptide (ANP) secretion. Eight beagles were subjected to rapid atrial pacing (AP) at 400 beats/min for 16 days. After complete recovery of left ventricular function, they underwent rapid ventricular pacing (VP) at 240 beats/min of equal duration. Left atrial systolic maximal dimension (LAmax) and left atrial appendage (LAA) peak late emptying velocity (LAA-E) were assessed by echocardiography. Blood samples were taken from the right atrium and from the peripheral vein. LAmax after AP and VP enlarged significantly (2.16 +/- 0.21 cm vs 2.41 +/- 0.23 cm, P = 0.002). Compared with baseline, LAA-E velocities were significantly reduced (0.65 +/- 0.12 m/s vs 0.26 +/- 0.16 m/s, P = 0.001) after AP only. AP caused a significant elevation of PRA in right atrial (9.28 +/- 4.23 nmol/L per hour) and peripheral samples compared with baseline values (4.82 +/- 2.53 nmol/L per hour, P = 0.04). ANP levels increased after AP (1117.12 +/- 252.21 fmol/L) with respect to baseline values (824.37 +/- 159.08 fmol/L, P = 0.001). There was no difference in PRA and ANP levels between atrial and peripheral samples. Atrial size and impaired systolic appendage function play an important role in secretion of PRA and ANP. Both neuro-humoral pathways may be therapeutic targets in the treatment of patients with AF.

Sympathetic reinnervation after heart transplantation, assessed by iodine-123 metaiodobenzylguanidine imaging, and heart rate variability.

OBJECTIVE: Complete allograft denervation occurs during heart transplantation. Partial ventricular sympathetic reinnervation may develop one year or later after transplantation and can be measured with iodine-123-meta-iodobenziylguanidine (MIBG) uptake. Aim of this study was to assess sinus node sympathetic reinnervation measured with heart rate variability and ventricular sympathetic reinnervation evaluated with MIBG. METHODS: Twelve patients and 14 healthy controls were included. In patients, MIBG scintigraphy with early and late imaging was performed. Heart to mediastinum ratio (HMR) was calculated and patients were divided in groups with (HMR>1.3) and without left ventricular reinnervation (HMR<1.3). Bipolar ECG with high sampling rate and resolution was recorded over 8.5 min in supine position and in upright position after 10 min interval. R-R intervals in time domain and heart rate variability in frequency domain through spectral power analysis of R-R intervals were analysed to evaluate sinus node reinnervation. Spectral power in low frequency range (0.04-0.15 Hz) above 4.5 ms(2) was considered as sinus node sympathetic reinnervation. RESULTS: Six (50%) patients had evidence of left ventricular sympathetic reinnervation on scintigraphy. Sinus node sympathetic reinnervation based on heart rate variability was detected in 6 (50%) patients in supine, and in 4 (33%) patients in upright body position. Four patients groups were discerned: (1) with ventricular and sinus node sympathetic reinnervation, (2) with sinus node sympathetic reinnervation, (3) with ventricular sympathetic reinnervation and (4) without atrial or ventricular sympathetic reinnervation. Ventricular reinnervation process was time dependent and sinus node reinnervation was not. CONCLUSIONS: Simultaneous ventricular sympathetic reinnervation assessed by MIBG and sinus node sympathetic reinnervation assessed by heart rate variability in supine as in upright position were detected only in two patients (17%). The results of our study show that eventual sinus node sympathetic reinnervation and left ventricular sympathetic reinnervation do not occur simultaneously.

Echocardiographic [correction of Ehocardiographic] evaluation of regional left atrial function after rapid atrial pacing.

Rapid regular atrial pacing (RAP) produces changes in atrial function similar to those caused by atrial fibrillation in animal models. Left atrial appendage (LAA) function represents regional atrial function. The aim of our study was to investigate the influence of RAP on left atrial regional function and to evaluate the reversibility of changes after termination of pacing in a canine model. Eight dogs were subjected to RAP (400 bpm) for 16 days. Transesophageal echocardiography was performed at baseline, immediately after RAP and 4 weeks after the termination of RAP. The LAA peak late emptying velocity (LAA-E) and filling wave (LAA-f) were measured. LAA-E velocities were significantly reduced and filling wave velocities (LAA-f) were significantly less negative after RAP compared with the baseline values. Four weeks after termination of pacing, the LAA-E and LAA-f velocities were normal. RAP results in impaired regional atrial systolic and diastolic function. The changes were completely reversible 4 weeks after termination of pacing. These results suggest that the LAA is mechanically stunned after RAP.

Impaired sinus node function and global atrial conduction time after high rate atrial pacing in dogs.

In animal and human studies, it has been shown that atrial fibrillation shortens the atrial refractory period and impairs its rate adaptation. The objective of this study was to evaluate the effects of high-rate pacing on sinus node function and intra-atrial conduction. Eight dogs were subjected to rapid atrial pacing (AP) at 400 bpm for 16 days. Sinus node recovery time (SNRT) and P-wave duration were measured at baseline, immediately after AP and four weeks after the termination of AP. SNRT immediately after AP was significantly prolonged at all pacing rates compared to the baseline values. P-wave duration was significantly longer after AP relative to the baseline values. All the variables were completely reversible four weeks after the termination of pacing. Rapid AP induces sinus node dysfunction and prolongs the intra-atrial conduction time. It is possible that the electrical remodelling extends to the sinus node as well.

Nicardipine diminished equinatoxin II-induced decrease of coronary flow in isolated rat and pig hearts.

Equinatoxin II (EqT II) is a basic, cardiotoxic polypeptide. The vasoconstrictory effect of the toxin on isolated porcine coronary arteries was diminished by nicardipine, an L-type calcium channel antagonist. A comparison was made of the effects of EqT II alone and EqT II in the presence of nicardipine on the coronary flow in porcine and rat hearts isolated according to Langendorff's method. In both models EqT II decreased coronary flow in a dose-dependent manner and there were no statistically significant differences between the two models (p>0.05). However, 1 M nicardipine diminished the effects of EqT II on coronary flow in isolated porcine hearts more than in isolated rat hearts (p<0.05). The results suggest that the activation of L-type calcium channels is one of the mechanisms involved in the lowering of coronary flow induced by EqT II.