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PTCA is now applied to patients with unstable acute ischemic syndromes, severe multivessel coronary artery disease, and impaired left ventricular function. To minimize the risk during angioplasty, several coronary and systemic circulation support approaches have been developed as adjuncts to high-risk angioplasty. Local coronary support techniques include the perfusion balloon catheter, the coronary stent, directional coronary atherectomy, laser balloon angioplasty, perfluorocarbon coronary perfusion, coronary sinus retroperfusion, and distal coronary hemoperfusion. Systemic circulatory support includes intraaortic balloon counterpulsation, cardiopulmonary support, the hemopump, and left heart partial bypass. These support devices, while associated with significant complications, may ultimately improve the safety of coronary angioplasty and allow its application to those who would otherwise not be candidates for revascularization.

Patients with paroxysmal atrial fibrillation (PAF) are prone to recurrence. We compared the efficacy and tolerability of flecainide acetate in the control of PAF by means of conventional treatment with quinidine in 19 patients without structural heart disease. A randomized, placebo-controlled, crossover protocol consisting of 8 weeks of treatment with either agent was used. The recurrence of PAF was documented in a symptom diary and confirmed by event ECG recording. Complete control of symptoms was achieved in 4 of 19 and 2 of 11 of patients with flecainide and quinidine, respectively. Both agents prolonged the time to the first recurrence and significantly reduced the total duration of PAF recurrence by 40% and 47%, respectively (p less than 0.05 compared with placebo). Compared with quinidine, flecainide significantly reduced the frequency of recurrence and the rate of PAF during a recurrent episode. However, treatment with flecainide was associated with a higher incidence of symptomatic sinus pauses and visual disturbances compared with a higher incidence of gastrointestinal side effects with quinidine. During a follow-up period of 32 months, satisfactory control was achieved in 74% of patients with the use of these two antiarrhythmic agents.

The effect of an abrupt reduction in atrial pressures on atrial natriuretic peptide (ANP) secretion was studied in four patients with complete atrioventricular block with a dual-chamber pacemaker when the pacing mode was changed from the VVI to the DVI mode at an equal rate of 70/min. Simultaneous continuous hemodynamic monitoring was performed using a balloon-tipped thermodilution catheter. With DVI pacing, there was an immediate decrease of right atrial pressure from 4.5 +/- 0.9 to 1.8 +/- 1.1 mm Hg, and a reduction of pulmonary arterial wedge pressure from 7 +/- 0.8 to 4.5 +/- 0.9 mm Hg, together with a rise in cardiac output from 3.1 +/- 0.2 to 3.7 +/- 0.2 L/min. However, despite a constant hemodynamic status after dual-chamber pacing, the arterial ANP level steadily decreased from 151 +/- 26 pg/ml to a steady low level of 78 +/- 15 pg/ml after 20 minutes of dual-chamber pacing (percentage reduction- 48 +/- 8%, p less than 0.05). This persisted until the end of the study at 60 minutes. The time-dependent decay in ANP secretion after an abrupt and constant change in hemodynamic status should be considered when interpreting ANP levels.

The effects of short- and long-term calcium replacement on myocardial function in six asymptomatic patients (age 48 +/- 3, mean +/- SEM) with hypocalcemia complicating surgical hypoparathyroidism were studied. Cardiac output was determined by ascending aortic continuous wave Doppler assessment and was measured as minute distance. During intravenous calcium replacement at rest, ascending aortic minute distance increased from 6.75 +/- 1.10 to 9.17 +/- 1.29 m as the calcium level rose from 1.76 +/- 0.08 to 2.06 +/- 0.19 mmol/L without changes in heart rate and blood pressure (p less than 0.01). The peak velocity and acceleration of blood flow derived from Doppler measurement showed a similar rise during calcium infusion. Symptom-limited cycle ergometry was performed before and 3 months after normalization of calcium by long-term oral therapy. Although the resting cardiac output was unchanged, the maximum cardiac output at peak exercise also increased from a minute distance of 11.58 +/- 1.84 to 15.37 +/- 2.28 m (p less than 0.05), together with an increase of maximum heart rate from 136 to 149 beats/min (p less than 0.05). Exercise duration was also prolonged from 11.9 +/- 2.9 to 13.0 +/- 2.8 minutes. Thus hypocalcemia impairs cardiac performance, but this impairment is reversible with calcium replacement.

Subclinical myocardial involvement frequently occurs in patients with systemic lupus erythematosus (SLE). In this study, left ventricular diastolic function was assessed in 58 patients (54 female and 4 male; mean age 32 +/- 11 years) and in 40 sex-matched and age-matched healthy control subjects (37 female and 3 male; mean age 33 +/- 9 years) by means of pulsed Doppler echocardiography. All subjects had no clinical evidence of overt myocardial disease or abnormal left ventricular systolic function. Compared with the control group, patients with SLE had significantly prolonged isovolumic relaxation time (62 +/- 12 vs 80 +/- 14 msec; p less than 0.01), reduced peak early diastolic flow velocity (peak E) (82 +/- 18 vs 76 +/- 16 cm/sec; p less than 0.05), increased peak late diastolic flow velocity (peak A) (45 +/- 7 vs 53 +/- 8 cm/sec; p less than 0.01), reduced E/A ratio (1.81 +/- 0.32 vs 1.46 +/- 0.29; p less than 0.001), and lower deceleration rate of early diastolic flow velocity (EF slope) (489 +/- 151 vs 361 +/- 185 cm/sec2; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Labetalol, a combined alpha- and beta-blocking agent, was administered to 12 patients (mean age 55 years) with idiopathic dilated cardiomyopathy to examine its effects on symptomatology and exercise performance. Studies were performed before treatment, after 8 weeks of placebo, and after 8 weeks of labetalol therapy in a randomized, crossover, double-blind design. The mean (+/- SEM) dose of labetalol for the group was 275 +/- 29 mg. Compared to treatment with placebo, the maximum duration of symptom-limited exercise was significantly prolonged with labetalol (580 +/- 72 seconds to 683 +/- 71 seconds; p less than 0.005). Both the resting and peak exercise heart rate and systolic blood pressure were significantly reduced. Ascending aortic blood flow velocity was also measured by continuous-wave Doppler technique during exercise. Compared to placebo, treatment with labetalol conferred no significant change in cardiac output at rest but significantly improved cardiac output at maximum exercise (14 +/- 3%; p less than 0.001). Doppler-derived peak aortic flow velocity, acceleration, and flow velocity integral were also significantly improved at maximum exercise. Systemic vascular resistance, as derived from mean blood pressure/cardiac output, was reduced by 12 +/- 3% and 16 +/- 3% at rest and at maximum exercise, respectively. New York Heart Association functional class was improved (3.2 +/- 0.2 to 2.2 +/- 0.3; p less than 0.005). No major side effects from labetalol were encountered. Thus labetalol improves symptomatology, exercise capacity, and exercise hemodynamics and reduces systemic vascular resistance in patients with idiopathic dilated cardiomyopathy.