Paul Schweitzer

Power Spectral Analysis of Heart Period Variability of Preceding Sinus Rhythm Before Initiation of Paroxysmal Atrial Fibrillation

Time domain analysis of heart period variability in patients without structural heart disease demonstrated increased parasympathetic modulation before paroxysmal atrial fibrillation (AF) occurring predominantly at night. However, diurnal differences in autonomic activity preceding AF episodes in a diverse patient population have not been assessed. Accordingly, we performed spectral analysis of heart period variability on Holter recordings during sinus rhythm preceding AF in 29 patients, 17 with night and 12 with day episodes. Samples taken 5, 10, and 20 minutes before AF onset were compared. Normalized high-frequency (HF) spectral power change was greater when comparing the interval 10 to 5 minutes with 20 to 10 minutes preceding AF in 26 of 29 patients (0.09 +/- 0.07 vs 0.03 +/- 0.02; p < 0.0001). HF spectral power increased before 3 of 12 AF episodes during the day compared with 15 of 17 AF episodes during the night (p = 0.001). Nocturnal AF episodes were preceded by increased HF spectral power in the 5- versus the 20-minute sample expressed as natural logarithm-transformed values (5.6 +/- 4.8 vs 4.2 +/- 4.0; p < 0.005) and normalized values (0.19 +/- 0.09 vs 0.10 +/- 0.07; p < 0.02), a decrease in low-frequency/HF ratio (1.05 +/- 0.61 vs 2.21 +/- 1.75; p < 0.05) and heart rate (60 +/- 13 vs 71 +/- 13 beats/min; p = 0.06). Structural heart disease was more common with daytime than nocturnal AF episodes (58% vs 18%, p < 0.05). In conclusion, HF spectral power change was increased preceding most AF episodes. However, diurnal differences were demonstrated. Contrary to daytime AF, increased parasympathetic activity preceded predominantly nocturnal AF, mostly in younger patients with structurally normal hearts.

Radiation therapy-induced cardiac injury

Radiation therapy is currently standard treatment for a number of malignancies, including Hodgkins disease. With the advent of techniques (e.g., subcarnial blocks) that limit the dose of radiation to which the heart is exposed, the incidence of radiation-induced heart disease can be minimized. However, a small percentage of patients will eventually suffer iatrogenic effects. Most commonly seen is pericardial disease, but valvular, conduction system, and coronary artery disease are also seen. Further, because these patients are now surviving longer after therapy, those effects with a longer latent period may be seen with increasing frequency.

Warfarin in haemodialysis patients with atrial fibrillation: what benefit?

Warfarin is commonly used to prevent stroke in patients with atrial fibrillation; however, patients on haemodialysis may not derive the same benefit from warfarin as the general population. There are no randomized controlled studies in dialysis patients which demonstrate the efficacy of warfarin in preventing stroke. In fact, warfarin places the dialysis patient at increased risk for haemorrhagic stroke and possibly ischaemic stroke. Additionally, warfarin increases the risk of major bleeding and has been associated with vascular calcification. Routine use of warfarin in dialysis for stroke prevention should be discouraged, and therapy should only be reserved for dialysis patients at high risk for thrombo-embolic stroke and carefully monitored if implemented.

The electrocardiographic diagnosis of acute myocardial infarction in the thrombolytic era

The 12-lead ECG remains a simple and inexpensive technique to diagnose AMI in its early phases. The diagnostic accuracy of the ECG depends upon the extent of myocardial necrosis and its localization. The ECG is most sensitive in patients with occlusion of the LAD artery, followed by the RCA and the left CFA. In 10% to 20% of patients with AMI the initial ECG either shows nonspecific changes or is normal. The correlation between the ECG and infarct-related artery varies according to the involved vessel. Classic ECG changes are seen in 90% of the LAD artery, in 70% to 80% of RCA, and in only 50% of CFA occlusions. A second important issue is the mechanism and clinical significance of reciprocal ST segment changes, which usually indicate larger MI, more impaired ventricular function, worse prognosis, and in some patients, significant disease of a noninfarct-related artery. Furthermore, the value of the ECG in estimating myocardial injury and infarct size remains controversial. The ECG plays an important role in coronary reperfusion. ST segment elevation is one of the principal criteria for instituting thrombolytic therapy, and helps predict those who will most likely benefit from coronary reperfusion. The role of the ECG in evaluating the reperfusion status after coronary thrombolysis is not clear. Rapid return to baseline or normalization of the ST segment suggests opening of the occluded vessel, though a small or negligible change does not exclude successful reperfusion.

Carotid sinus hypersensitivity: Case report and review of the literature

Carotid sinus hypersensitivity is a potentially treatable cause of recurrent neurologic symptoms. Diagnosis depends upon recognizing the variable presentation of symptomatic carotid sinus hypersensitivity, and noting an exaggerated cardiovascular response to carotid sinus massage associated with neurologic symptoms. Once the diagnosis of symptomatic carotid sinus hypersensitivity has been established, it is important to delineate the type of hypersensitivity present, because identification of the vasodepressor response has important therapeutic implications.

Telemetry monitoring guidelines for efficient and safe delivery of cardiac rhythm monitoring to noncritical hospital inpatients.

Telemetry monitoring is a limited resource in most hospitals. Few clinical studies have established firm criteria for inpatient telemetry. At our urban institution, we have developed and incorporated guidelines to identify patients who benefit from cardiac rhythm monitoring. These guidelines serve to minimize inappropriate use of telemetry beds, thereby preventing emergency department overcrowding and ambulance diversion. This improvement in efficiency is achieved without compromising health care.

ST-segment depression in aVr as a predictor of culprit artery and infarct size in acute inferior wall ST-segment elevation myocardial infarction

BACKGROUND ST-segment depression in lead aVR in acute inferior wall ST-segment elevation myocardial infarction (STEMI) has recently been suggested as a predictor of left circumflex (LCx) artery involvement. The purpose of this study is to evaluate the clinical significance of aVR depression during inferior wall STEMI. METHODS This study included 106 consecutive patients who presented with inferior wall STEMI and underwent urgent coronary angiogram. Clinical and angiographic findings were compared between patients with and without aVR depression > or = 0.1 mV. RESULTS The sensitivity and specificity of aVR depression as a predictor of LCx infarction were 53% and 86%, respectively. In patients with right coronary artery infarction, aVR depression was associated with increased cardiac enzymes and the involvement of a large posterolateral branch, which may explain the larger infarction. CONCLUSIONS ST-segment depression in lead aVR in inferior wall STEMI predicts LCx infarction or larger RCA infarction involving a large posterolateral branch.

Acute pulmonary edema after cardioversion of cardiac arrhythmias

OBJECTIVE To examine the occurrence of acute pulmonary edema after cardioversion of arrhythmias. METHODS Cases, case series, and related articles on the subject identified through a comprehensive literature search were examined. RESULTS Thirty cases (23 males) of post cardioversion acute pulmonary edema were identified. The mean age was 53.8 +/- 13 years (range, 18 to 75 years). Underlying arrhythmias were atrial fibrillation (69%), atrial flutter (24%), supraventricular tachycardia (4%), and ventricular tachycardia (4%). The duration of arrhythmia preceding cardioversion varied widely ranging from 1 day to 13 years. Twenty-six (87%) patients had concomitant cardiovascular disease comprising of coronary artery disease (38%), rheumatic heart disease (23%), cardiomyopathy (23%), and hypertension (8%). Direct current electrical cardioversion was used in 28 (93%) patients and pacing in two (7%) patients. Occurrence of pulmonary edema was independent of the amount of energy used for cardioversion (range 20 to 1280 Joules, mean 263 +/- 27 Joules). Short acting general anesthetic drugs were administered in 14 (47%) and sedation in eight (27%) patients. Sinus rhythm was established in 23 (77%) patients. Duration to develop pulmonary edema after cardioversion was available in 23 patients and ranged from immediately to 96 h. Pulmonary edema occurred within 15 min after cardioversion in 22%, within 3 h in 30%, within 24 h in 30%, within 48 h in 17% and within 96 h in remaining 4% of patients. Three patients required mechanical ventilation. CONCLUSION The rare complication of acute pulmonary edema after cardioversion has been reported mostly in patients with underlying cardiac disease, and is independent of the amount of energy used for cardioversion.

Long-term antiarrhythmic therapy: Problem of low drug levels and patient noncompliance

Maintenance of adequate serum blood levels is crucial to successful antiarrhythmic therapy. Serum levels of four antiarrhythmic agents (long-acting procainamide, quinidine sulfate, quinidine gluconate, and disopyramide) were determined in 98 consecutive ambulatory patients receiving long-term oral therapy. Medication dosages, dosing intervals, and time elapsed from last dosage until blood sampling were determined. Seventy-five patients (76.5 percent) had subtherapeutic blood levels (with mean levels less than 50 percent of the suggested minimum), and only 22 patients (22.5 percent) had therapeutic levels. Even among the 61 patients who claimed to have taken their medications within the six hours prior to blood sampling, 43 (70 percent) had subtherapeutic levels. These ratios held among all subgroups studied. Physicians should be aware of the high proportion of patients receiving long-term oral antiarrhythmic therapy with inadequate serum blood levels when planning therapeutic regimens.

The effect of statin therapy on ventricular tachyarrhythmias: a meta-analysis

The objective of this study was to assess whether statin therapy is associated with a reduction in ventricular tachyarrhythmias. Statins have been shown to be beneficial beyond their cholesterol-lowering effects. These pleiotropic effects have been implicated in the protection against atrial fibrillation and the reduction in appropriate implantable cardioverter–defibrillator therapy in patients with coronary artery disease. This meta-analysis was conducted to evaluate whether statins were associated with a reduction in ventricular tachyarrhythmias in patients with coronary artery disease or nonischemic cardiomyopathy. The Medline and Cochrane databases were searched for studies in human subjects published in the English language between 1985 and February 2010. Studies were included in our analysis if they provided data regarding the association between the use of statins and the incidence of ventricular tachycardia/ventricular fibrillation (VT/VF) in patients with coronary artery disease or nonischemic cardiomyopathy. The occurrence of ventricular arrhythmias was defined as the VT/VF occurrence or appropriate implantable cardioverter–defibrillator therapy for VT/VF. Of the 166 identified articles, nine prospective studies with 150,953 patients enrolled met our inclusion criteria and were included in this analysis. Using a random effects model, statin therapy was associated with a 31% reduction in the risk of VT/VF when compared with the group not on statin therapy (pooled relative risk = 0.69, 95% confidence interval, 0.58–0.83; heterogeneity I2 = 57.3%). There was a low likelihood of publication bias in this analysis (Eggers test P = 0.957). Statin use in patients with coronary artery disease or nonischemic cardiomyopathy is associated with a 31% reduction in the development of ventricular tachyarrhythmias.