Use of intravenous adenosine as a noninvasive diagnostic test for sick sinus syndrome.

BACKGROUND: Testing for sick sinus syndrome (SSS) requires invasive stimulation protocols for sinus node recovery time (SNRT) and corrected sinus node recovery time (CSNRT). METHODS AND RESULTS: We compared the CSNRT with the lengthening of the sinus cycle length (ADO:SCL) corrected to the basic cycle length (ADO:CSNRT) after administration of an intravenous bolus of adenosine (0.15 mg/kg) in 10 patients with clinical SSS (group 1) and 67 control patients (group 2). With 550 ms as an abnormal result for the ADO:CSNRT (and for the CSNRT) as an indicator of sinus node dysfunction, the ADO:CSNRT had a sensitivity of 80% and specificity of 97% for detection of SSS compared with sensitivity and specificity of 70% and 95% for invasive CSNRT. When combined, the 2 tests had a sensitivity of 100%. There was significant difference in the CSNRT between group 1 (1848 +/- 1825 ms) and group 2 (355 +/- 169 ms, P <. 0001) and a significant difference in ADO:CSNRT between group 1 (1168 +/- 1002 ms) and group 2 (272 +/- 592 ms, P <.0001). CONCLUSIONS: We conclude that the ADO:CSNRT is a sensitive and specific test for SSS that equals invasive testing and should be considered as an alternative to invasive testing in patients with suspected SSS.

Mechanical dysfunction of the left atrium and the left atrial appendage following cardioversion of atrial fibrillation and its relation to total electrical energy used for cardioversion.

In 39 patients undergoing electrical cardioversion for atrial fibrillation (AF), we examined the effect of total electrical energy used for cardioversion on postcardioversion peak left atrial (LA) rapid filling velocity (A) and the atrial emptying fraction, and recovery of LA effective mechanical atrial function (defined as peak A velocity > or = 0.50 m/s), as assessed by transthoracic echocardiography. In a subset of 27 patients who underwent pre- and postcardioversion transesophageal echocardiography, we assessed the relation between total electrical energy and LA appendage filling and emptying velocities and spontaneous echo contrast. Patients were randomized to receive an initial shock of 1.5 J/kg based on body weight, or 2.5, 3.5, 5 J/kg, or 360 J, followed sequentially by higher shock intensities until sinus rhythm was achieved. Patients were classified into 4 groups based on quartiles of total energy delivered for cardioversion. Conversion to sinus rhythm was associated with a significant decrease in the LA appendage filling velocities (0.42 +/- 0.20 m/s vs 0.29 +/- 0.14 m/s; p = 0.002) and LA appendage emptying velocities (0.40 +/- 0.22 m/s vs 0.29 +/- 0.18 m/s; p = 0.03), but no change in the incidence of spontaneous echo contrast (61% vs 70%, p = 0.08). The 4 groups of patients did not differ with respect to postcardioversion LA appendage filling velocities, LA appendage emptying velocities, incidence of spontaneous echo contrast, or worsening of spontaneous echo contrast. Similarly, the change in LA appendage filling and emptying velocities associated with cardioversion was not different between the groups. Furthermore, postcardioversion peak A velocity and atrial emptying fraction and recovery of effective mechanical atrial function were similar between the 4 groups. These results suggest that in patients undergoing electrical cardioversion for AF, the total electrical energy used for cardioversion has no effect on the mechanical function of the left atrium or LA appendage following cardioversion.

Clinical variables affecting recovery of left atrial mechanical function after cardioversion from atrial fibrillation.

OBJECTIVES: We sought to evaluate the effect of clinical factors on recovery of atrial function after cardioversion for atrial fibrillation. BACKGROUND: Lack of effective mechanical atrial function (EMAF) after cardioversion of atrial fibrillation predisposes to thromboembolic complications and delays improvement in functional capacity. METHODS: Fifty-two patients underwent cardioversion (group I, electrical cardioversion, n = 40; group II, pharmacologic or spontaneous cardioversion, n = 12) for atrial fibrillation. Serial transmitral inflow Doppler variables were recorded after cardioversion until EMAF (atrial filling velocity > 0.50 m/s) was seen. Clinical variables (age, duration of atrial fibrillation, left ventricular ejection fraction, left atrial diameter, underlying cardiovascular disease, antiarrhythmic drug therapy and mode of cardioversion) were tested for an association with the outcomes of recovery of atrial function by day 3 and day 7. RESULTS: Effective mechanical atrial function recovered in 68% of patients by day 3 and in 76% by day 7 after cardioversion. The mode of cardioversion was significantly associated with recovery of atrial function by day 3 in bivariate and multivariate analyses (odds ratio 0.12, 95% confidence interval 0.01 to 1.0, for electrical cardioversion). None of the variables had an association with recovery of atrial function by day 7. Group I patients took a longer time to recover atrial function than group II patients (p = 0.012). In addition, group I patients had a significantly lower peak atrial filling velocity (mean [+/-SD] 0.39 +/- 0.19 m/s vs. 0.56 +/- 0.16 m/s) and a higher early filling to atrial filling velocity ratio (2.5 +/- 1.2 vs. 1.5 +/- 0.5) after cardioversion. CONCLUSIONS: A high proportion of patients recover EMAF within 1 week after cardioversion. Patients who undergo electrical cardioversion display a greater degree and a longer duration of mechanical atrial dysfunction than those who convert pharmacologically or spontaneously.

The signal-averaged electrocardiogram in cardiac transplantation. A noninvasive marker of acute allograft rejection.

Cardiac allograft rejection represents a major cause of morbidity and mortality in transplanted patients. Noninvasive markers of rejection have been sought, though transvenous endomyocardial biopsy remains the "gold standard" for the diagnosis of rejection. Sixty-one signal-averaged electrocardiograms (five in patients with rejection and 56 in patients without rejection) were obtained on 41 patients and prospectively analyzed in frequency domain via fast Fourier transform (FFT). Patients with acute allograft rejection demonstrate a significant increase in the high-frequency components of the QRS complex upon FFT analysis (QRS area ratio 203 +/- 57 vs. 66 +/- 10, P = 0.0007) compared with patients without rejection. Thus, frequency domain analysis may be a useful noninvasive marker of acute cardiac allograft rejection.

The clinical use of class IC antiarrhythmic drugs.

Flecainide, encainide, and propafenone belong to class IC antiarrhythmic drugs. They are new and potent drugs which markedly depress Phase 0 of the action potential without affecting repolarization. Class IC drugs are very potent suppressors of premature ventricular complexes but their efficacy in the treatment of ventricular tachycardia is only comparable to that of class IA agents. Although noncardiac side effects are minimal, myocardial depression and serious proarrhythmic effects are not infrequently noted. A thorough understanding of the pharmacodynamics and toxicity potential of these drugs is therefore essential for their safe usage.

The usefulness of head-up tilt testing and hemodynamic investigations in the workup of syncope of unknown origin.

To enhance the clinical evaluation of patients suffering from recurrent syncope of unknown origin, the integrity of mechanisms controlling blood pressure was examined in 151 patients utilizing a screening tilt test. Ninety-eight patients had an abnormal blood pressure and/or heart rate response to tilt testing, including provoked syncopal attacks in 63 patients. Whenever indicated, the screening tilt test was followed by blood volume and hemodynamic determinations, as well as autonomic nervous system testing to identify contributing pathophysiological abnormalities (hypovolemia, venous pooling, autonomic dysfunction). Detailed analysis of this battery of tests allowed us to conclude that: (1) The tilt test is commonly a provocative tool in the workup of patients with recurrent syncope due to vasovagal - vasodepressor reactions and other abnormalities of blood pressure regulation; (2) Its usefulness is augmented by associated hemodynamic and blood volume evaluations; (3) The identification of contributory pathophysiological mechanisms of blood pressure control facilitates specific therapeutic interventions.

Clinical and systemic hemodynamic effects of nitrendipine.

The antihypertensive effects of nitrendipine were evaluated in 12 subjects with hypertension, one of whom could not tolerate the drug for more than 3 days; hence hemodynamics were studied in the 11 subjects who were treated for 2 wk. In one patient taking 40 mg twice a day, blood pressure reduction was associated with a hemodynamic pattern of hyperkinetic circulation. Of the other 10 subjects, all of whom were taking 20 mg twice a day, two did not respond, but 8 had significant reduction in mean arterial pressure (136 +/- 4.3 to 106 +/- 3.2 mm Hg) resulting from a decrease in total peripheral resistance (52 +/- 3.7 to 35 +/- 2.6 U X m2). Changes in cardiac output, heart rate, and cardiopulmonary volume varied widely among subjects, such that average changes did not attain significance. Heart rate and cardiopulmonary volume, however, changed in the same direction, which suggests that the alterations in both were related to the degree of reflex sympathetic stimulation induced by nitrendipine. Plasma renin activity (PRA) increased during treatment (2.6 +/- 1.0 to 9.3 +/- 4.1 ng/ml/hr), whereas the increase in plasma aldosterone (PA) levels did not attain significance (13.7 +/- 1.6 to 21.5 +/- 4.5 ng/dl). As a result, PA/PRA decreased (16.1 +/- 4.9 to 9.4 +/- 2.6). These results suggest that calcium entry blockade might have interfered with steroidogenesis, thus blunting the effect of increased PRA. Finally, blood pressure response to nitrendipine in the whole group correlated inversely with pretreatment PRA (r = -0.88), suggesting greater activity of the drug in low-renin hypertension.

Determinants of left ventricular hypertrophy and function in hypertensive patients. An echocardiographic study.

Hypertensive patients present a wide spectrum of echocardiographic alterations. A review of these changes in 74 patients (37 untreated and 37 treated) revealed left ventricular hypertrophy in 43 (58 percent). There was no significant difference between treated and untreated patients in regard to either the prevalence of left ventricular hypertrophy or of its various subtypes [concentric left ventricular hypertrophy in 15 (20.3 percent), asymmetric septal hypertrophy in 16 (21.6 percent), and combined left ventricular hypertrophy and dilation in 12 (16.2 percent)]. None of the patients who showed asymmetric septal hypertrophy had abnormal motion of the mitral valve. Cardiac performance as judged by left ventricular percent shortening was related inversely to end-systolic stress (p less than 0.001) and positively to the ratio of end-systolic pressure/end-systolic volume (an index of myocardial contractility) (p less than 0.01). Multiple regression analysis showed an increased dependence on afterload (end-systolic stress), when left ventricular hypertrophy developed and especially when it was associated with left ventricular dilation.