Soad Bekheit

Use of heart rate spectral analysis to study the effects of calcium channel blockers on sympathetic activity after myocardial infarction

We used spectral analysis of heart rate variability (HRV) to study the effects of the calcium channel blockers diltiazem and nifedipine and the beta-blocker metoprolol on the sympathetic nervous system in patients following myocardial infarction. Energy in the low-frequency range (0.04 to 0.12 Hz) in the standing (tilt) position was used as a quantitative index of sympathetic activity. Twenty-seven male patients, mean age 62 +/- 13 years, were studied 2 to 6 weeks after myocardial infarction. Eight patients received metoprolol, 100 mg twice daily; nine patients received diltiazem, 60 mg three times daily; and 10 patients received nifedipine, 10 mg three times daily. HRV and arterial blood pressure were recorded before and 5 to 7 days after initiation of therapy. None of the drugs had significant effects on the systolic blood pressure, and only nifedipine significantly reduced the diastolic blood pressure. Metoprolol and diltiazem reduced the low-frequency HRV in all patients studied, but nifedipine had no consistent effects. Our results suggest that diltiazem had a depressant effect on sympathetic activity similar to beta-adrenergic blockers. This effect was not observed with nifedipine. The reduction in sympathetic activity by diltiazem may contribute to its therapeutic effects in the post-infarction period.

Recordings of diaphragmatic electromyograms during cryoballoon ablation for atrial fibrillation accurately predict phrenic nerve injury.

BACKGROUND Cryoballoon ablation has been associated with a significant incidence of phrenic nerve injury (PNI). OBJECTIVE The purpose of this study was to evaluate whether recordings of diaphragmatic compound motor action potentials (CMAP) on a modified lead I during cryoballoon ablation can predict PNI. METHODS Cryoballoon ablation was performed in 109 patients with atrial fibrillation (AF). During ablation of the right-sided pulmonary veins, the phrenic nerve was paced from the superior vena cava. The right and left arm electrodes from a 12-lead ECG were positioned 5 cm above the xiphoid process and 16 cm along the right costal margin. The amplitude of CMAP was recorded on lead I during ablation. RESULTS Cryoballoon was applied 424 times in 211 right-sided veins. PNI occurred in 7 (6.4%) patients. The average CMAP amplitude did not significantly change in patients without PNI from the initial average CMAP amplitude of 0.34 ± 0.18 mV to 0.32 ± 0.17 mV (P = .58). In patients who developed PNI, there was a significant decrease in the initial average CMAP amplitude during the ablation from 0.33 ± 0.14 mV to 0.09 ± 0.05 mV (P <.001). The maximal percent change in the average CMAP amplitude in patients with PNI was higher (70% ± 10%) than in patients without PNI (7.6% ± 7%; P <.001). In any patient without PNI, the CMAP amplitude did not decrease more than 35% from baseline. CONCLUSION Recording of CMAP amplitude on a modified lead I is reliable and could be early and sensitive method for predicting PNI in patients undergoing cryoballoon ablation for AF.

Use of Intracardiac Echocardiography for Early Detection of Phrenic Nerve Injury During Cryoballoon Pulmonary Vein Isolation

Use of Intracardiac Echocardiography for Early Detection of Phrenic Nerve Injury.  Cryoballoon catheter ablation has recently emerged as an effective tool to achieve pulmonary vein isolation (PVI). Right‐sided PVI with cryoballoon ablation has been associated with a significant incidence of phrenic nerve palsy. Multiple modalities are currently utilized to monitor phrenic nerve function during ablation. We describe a novel approach toward monitoring and diagnosing phrenic nerve palsy using intracardiac echocardiography (ICE) during cryoballoon ablation of the right pulmonary veins. This technique of monitoring has the advantage of continuous direct diaphragmatic visualization without the use of fluoroscopy, hence significantly minimizing radiation to both the patient and the operator. In addition, this technique does not require extra personnel to monitor the diaphragm using manual palpation. Further prospective studies of our and other methods for prevention of phrenic nerve palsy are required. (J Cardiovasc Electrophysiol, Vol. 23, pp. 874‐876, August 2012)

Safety and efficacy of second-generation versus first-generation cryoballoons for treatment of atrial fibrillation: a meta-analysis of current evidence

BackgroundThe newer second-generation cryoballoons (CB-2 or Arc-Adv-CB) have been shown to achieve significantly lower temperature and faster pulmonary vein isolation (PVI) time in comparison with first-generation cryoballoons (CB-1 or Arc-CB). To test the premise that second-generation cryoballoons can improve clinical outcomes in comparison to first-generation cryoballoons in terms of safety and efficacy, we pooled data for systemic review and meta-analyses from all available literature comparing their clinical performance.MethodsThe Cochrane Library, PubMed, Google Scholar, and studies presented at various meetings were searched for any published literature comparing safety and efficacy of the second-generation cryoballoons (Arctic Front Advance cryoballoons) with first-generation cryoballoons (Arctic Front Cryoballoons). A total of ten published studies, with 2310 patients, were included in this meta-analysis with 957 patients in second-generation cryoballoon group and 1237 patients in first-generation cryoballoon group.ResultsThe pooled analysis showed significant superiority of second-generation cryoballoons in terms of less procedure time, less fluoroscopic time, and fewer incidences of arrhythmia recurrences compared to first-generation cryoballoons at the cost of higher incidence of persistent and transient phrenic nerve palsy. The differences in the rate of pericardial effusion and incidence of access site complications were not statistically significant.ConclusionsSecond-generation cryoballoons are associated with a shorter procedure time and fluoroscopy time, along with lower arrhythmia recurrence rates, reflecting higher procedure efficacy when compared to first-generation cryoballoons. However, they are also associated with a higher incidence of transient and persistent phrenic nerve palsies with a non-significant difference in rates of access site complications and pericardial effusion.

Ginseng: a potential cause of long QT.

Ginseng is a frequently used food additive and considered to be relatively safe. Long QT syndrome can be hereditary or acquired. It presents as syncope, sudden cardiac death, or seizures. We report the novel case of a female patient without cardiovascular risk factors who developed prolonged QT with subsequent torsades de pointes during periods in which she was drinking large amounts of ginseng.

Pantoprazole (Proton Pump Inhibitor) Contributing to Torsades de Pointes Storm

Proton pump inhibitors (PPI), commonly used medications for peptic ulcer prophylaxis, have been recently described to cause hypomagnesemia through both urinary and gastrointestinal losses. Very few reports have linked hypomagnesemia with life-threatening ventricular arrhythmias. However, these reports included patients with other complex medical problems that may have also contributed to these arrhythmias. To our knowledge, ventricular arrhythmias associated with hypomagnesemia induced by proton pump inhibitors have never been reported. We present a case of a 53-year-old chronic alcoholic male patient, who was started on a proton pump inhibitor for peptic ulcer prophylaxis, which resulted in resistant hypomagnesemia associated with a storm of life-threatening arrhythmias, namely Torsades de Pointes (TdP). A 53-year-old man with no previous cardiac history was brought by Emergency Medical Services with a chief complaint of palpitations and dizziness for 1 day. His only significant medical history was chronic alcohol abuse and was not taking any medications before his admission. His physical examination was normal, except for an irregularly irregular rapid pulse and a blood pressure of 157/104 mm Hg. The ECG on admission showed atrial fibrillation with rapid ventricular response at an average of 190 beats per minute. Admitting routine labs showed normal complete blood counts. Electrolyte laboratory values revealed 136 mEq/L of sodium, 4.6 mmol/L of potassium, 100 mEq/L of chloride, 16 mEq/L of bicarbonate, 11 mg/dL of blood urea nitrogen, 0.68 mg/dL of creatinine, 9 mg/dL of calcium, and 1.5 mg/dL of magnesium. He was started on intravenous diltiazem for rate control and intravenous heparin for anticoagulation. Routine oral pantoprazole 40 mg once daily was also prescribed for peptic ulcer prophylaxis. Seven hours later, while on telemetry, the patient became unresponsive. The telemetry rhythm …

Inadvertent malposition of a permanent pacemaker ventricular lead into the left ventricle which was initially missed and diagnosed two years later: a case report.

IntroductionInadvertent malposition of a pacemaker ventricular lead into the left ventricle is an uncommon event, and its actual incidence is probably unknown. It may be underestimated and underreported because of a possible asymptomatic course. A 12-lead electrocardiogram is important to confirm proper placement.Case presentationWe report a case of a 60-year-old Caucasian man with a malpositioned transvenous permanent pacing lead into the left ventricle via a patent foramen ovale that was not suspected during implantation and went undiagnosed for two years without complications. The patient remained asymptomatic as he was being treated with oral anticoagulation therapy for atrial fibrillation. The decision was made to leave the pacing lead in place and continue lifelong warfarin therapy.ConclusionsInadvertent insertion of pacing wires into the left ventricle is a potentially dangerous complication that may happen under fluoroscopic guidance and may be overlooked by routine pacemaker interrogation. It is advisable to obtain a 12-lead electrocardiogram during or immediately after transvenous pacemaker implantation rather than use a routine pacemaker interrogation or a limited electrocardiogram.

The effects of smoking on myocardial conduction in the human heart

Inhalation of a few puffs on a cigarette increases the velocity of conduction and shortens the effective refractory period of the A-V node. These effects are attributed to adrenergic stimulation produced by minute amounts of nicotine absorbed. Wenckebach block is abolished whether induced by atrial pacing or occurring spontaneously. Conduction velocity in the His-Purkinje system and in the anomalous pathways in the WPW syndrome were not affected. Smoking increases the ventricular rate in atrial fibrillation, and antagonizes the cholinergic effects of digitalis.

Right Coronary Artery Fistula as a Result of Delayed Right Atrial Perforation by a Passive Fixation Lead

Delayed lead perforation (DLP) is an uncommon complication of permanent pacemaker and defibrillator implantation, especially that of the right atrium (RA).1 Lead perforation is considered delayed when it occurs >30 days after implantation. The incidence of DLP has been reported to be ≈0.8% and is more common in elderly individuals.1,2 With the yearly increase in implanted devices, and the advance in imaging modalities, this complication is more likely to be encountered. To our knowledge, delayed right atrial perforation involving a passive fixation lead remains extremely rare and has never been reported. We describe a case of an asymptomatic right atrial DLP resulting in a pseudoaneurysm and right coronary artery (RCA) fistula, diagnosed incidentally 53 months after the implantation of a passive atrial lead. Our patient is a 67-year-old man with a medical history of hypertension, diabetes mellitus, end-stage renal disease on hemodialysis, coronary artery bypass grafting, and ischemic cardiomyopathy. The patient had a dual-chamber implantable cardioverter-defibrillator implanted for primary prevention of sudden cardiac death. A passive fixation lead (5594 CapSureR SP Novus, Medtronic; Indianapolis, IN) was implanted in the RA appendage, and the right ventricular lead (6949 Sprint Fidelis, Medtronic) was implanted in the apical septum without difficulty. The initial atrial pacing threshold was 0.5 V at 0.4 ms and 1.5 V at 0.4 ms for the ventricular lead. The initial …

Takotsubo Cardiomyopathy precipitated by opiate withdrawal

INTRODUCTION Takotsubo Cardiomyopathy is a transient non-ischemic cardiomyopathy usually characterized by apical ballooning of the left ventricle, with electrocardiographic changes and enzyme release, without evidence of obstructive coronary artery disease. Typically seen in stress induced situations, in post-menopausal females, this condition may have a predilection for patients with dependency disorders. CASE The following is a case in which Takotsubo Cardiomyopathy was induced by withdrawal from opiate medications. Followed by resolution of symptoms after restarting maintenance opioid therapy. DISCUSSION We feel health care professionals should be aware of this possibility in such a patient population especially when they have demonstrated cardiovascular symptomatology. Given the prevalence of opiate use both recreational and iatrogenic, the index of suspicion for opiate-withdrawal induced cardiomyopathy should be high in the presence of cardiac symptomatology.