Clinical applications of programmed electrical stimulation of the heart.
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Arrhythmias, Cardiac↗
Biomedical subjects
E Andries
Publications and source records attributed to E Andries.
Impaired relaxation of the hypertrophied left ventricle in aortic stenosis: effects of aortic valvuloplasty and of postextrasystolic potentiation.
Impaired left ventricular (LV) filling in aortic stenosis (AS) is explained by slow LV pressure decay, which impedes LV inflow. This slow LV pressure decay could be explained by the altered myocardial wall stress pattern of AS or by a failure of inactivation of hypertrophied myocardium. To evaluate whether altered LV loading or impaired myocardial inactivation is the predominant control of LV relaxation and filling in AS, we studied the effects of aortic valvuloplasty (PTAV) and of postextrasystolic potentiation (PESP). LV micromanometer tip pressure recordings and simultaneous LV angiograms were obtained before and after PTAV in 10 patients with AS. PTAV reduced peak-to-peak aortic valve gradient from 101 +/- 7 to 40 +/- 5 mmHg (P less than 0.01), peak LV systolic pressure from 211 +/- 8 to 169 +/- 4 mmHg (P less than 0.01) and LV end-diastolic pressure from 22 +/- 3 to 13 +/- 2 mmHg (P less than 0.01). Despite these large drops of LV loading after PTAV, the time constant, T, of LV pressure decay decreased only slightly from 47 +/- 4 to 44 +/- 4 ms (P less than 0.05) and the LV peak filling rate remained unaltered. The influence of PESP on LV relaxation and filling was investigated in patients with AS using LV micromanometer tip pressures (n = 22) and simultaneous mitral valve Doppler echocardiograms (n = 9). After PESP the time constant, T, of isovolumic LV pressure decay increased from 43 +/- 4 to 54 +/- 4 ms (P less than 0.01).2+ 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Aortic Valve↗
Postextrasystolic potentiation worsens fast filling of the hypertrophied left ventricle in aortic stenosis and hypertrophic cardiomyopathy.
Impaired left ventricular (LV) filling in aortic stenosis (AS) and in hypertrophic cardiomyopathy (HCM) is caused by slow LV pressure decay, which could be explained by depressed inactivation of hypertrophied myocardium. Postextrasystolic potentiation (PESP), which increases activator calcium, could lead to further deterioration of LV relaxation. The influence of PESP on LV filling dynamics was, therefore, investigated in normal controls and in patients with LV hypertrophy caused by AS or by HCM. LV hemodynamics and LV hemodynamic relaxation indexes were determined during normal sinus rhythm (NSR) and after PESP. LV pressures were recorded by micromanometer tip catheters (controls, n = 10; AS, n = 17; HCM, n = 11). Simultaneous mitral flow Doppler echocardiograms were obtained in patients with LV hypertrophy (AS, n = 8, HCM, n = 5). Despite significant increases of LV dP/dtmax after PESP in all three study groups, PESP affected LV hemodynamic relaxation indexes differently. The time constant of LV pressure decay (TPB) derived from exponential curve fits with nonzero asymptote pressure remained unaltered after PESP in normal controls, rose from 62 +/- 17 to 74 +/- 21 msec (p less than 0.02) in patients with AS, and rose from 74 +/- 18 to 84 +/- 19 msec (p less than 0.02) in patients with HCM. Early diastolic LV pressure decay was measured by phi (phase of the first harmonic of a Fourier transform applied to the diastolic LV pressure waves) and by t (time interval from LV dP/dtmin to LV minimum diastolic pressure). After PESP, phi remained unaltered in normal controls but decreased in AS from 42.8 +/- 19.1 degrees to 24.0 +/- 28.8 degrees (p less than 0.001) and in HCM from 39.7 +/- 15.4 degrees to 26.9 +/- 15.7 degrees (p less than 0.001). Similarly, t was unchanged after PESP in normal controls but prolonged in AS from 146 +/- 48 to 205 +/- 86 msec (p less than 0.001) and in HCM from 168 +/- 40 to 208 +/- 53 msec (p less than 0.02).(ABSTRACT TRUNCATED AT 400 WORDS)
Adult↗
Dilatation of stenotic aortic valves through a temporary vascular prosthesis on the subclavian artery.
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Aged↗
Effects of long-term treatment with amiodarone on exercise hemodynamics and left ventricular relaxation in patients with hypertrophic cardiomyopathy.
The influence of long-term treatment with amiodarone on exercise hemodynamics and on left ventricular relaxation was studied prospectively in patients with hypertrophic cardiomyopathy. Rest-exercise hemodynamics (n = 9) and echocardiographic relaxation indexes (isovolumic relaxation time, dPW/dt) (n = 11) were measured in control conditions and after 5 weeks of oral amiodarone treatment (600 mg daily first week, 400 mg daily second week, 200 mg daily afterwards). Long-term amiodarone treatment in patients at rest caused a significant drop in heart rate from 80 +/- 11 to 75 +/- 11 beats/min (p less than .05), a rise in mean pulmonary artery pressure from 19 +/- 7 to 25 +/- 10 mm Hg (p less than .02), and a rise in mean pulmonary capillary wedge pressure from 11 +/- 4 to 17 +/- 8 mm Hg (p less than .05). Systemic arterial pressure, cardiac output, and systemic vascular resistance remained unaltered. Exercise tolerance assessed by serial supine bicycle stress testing was reduced in six of nine patients. Amiodarone treatment caused a significant rise in pulmonary capillary wedge pressure from 22 +/- 8 to 37 +/- 9 mm Hg (p less than .001) at the highest identical workloads and from 26 +/- 10 to 37 +/- 9 (p less than .005) at maximal symptom-limited workloads. Similarly, mean pulmonary artery pressure rose from 37 +/- 15 to 51 +/- 18 mm Hg (p less than .01) at highest identical workloads and from 42 +/- 19 to 51 +/- 18 mm Hg (p less than .01) at maximal symptom-limited workloads. There were no significant differences at maximal exercise level in heart rate, systemic arterial pressure, cardiac output, or exercise factor. Echocardiographic studies performed before and during long-term amiodarone treatment revealed no change in isovolumic relaxation time, end-diastolic or end-systolic posterior wall thickness, and peak posterior wall thinning rate. A negative inotropic action of amiodarone could explain the worsened rest and exercise hemodynamics observed during long-term treatment of patients with hypertrophic cardiomyopathy. Echocardiographic relaxation indexes remained unaltered despite the elevated left ventricular filling pressures. This finding could suggest a deleterious effect of amiodarone on myocardial inactivation, possibly similar in mechanism to the depressed myocardial inactivation observed in hypothyroidism.
Adult↗
Efficacy and tolerance of intravenous flecainide in patients with chronic high frequency ventricular arrhythmias.
The effectiveness and safety of intravenous flecainide was evaluated in 33 patients with chronic high frequency premature ventricular complexes (mean value of PVCs 23.7 min-1). Flecainide was injected intravenously at a rate of 20 mg per 2 min until complete disappearance of ventricular arrhythmias or up to a total dose not exceeding 200 mg. Total suppression of PVCs occurred in 31 out of 33 patients at the end of the injection (mean dose 132 mg). The overall reduction of PVCs was 94 per cent (P less than 0.001) at the end of infusion and 74 per cent (P less than 0.001) 1 h later. The mean plasma drug level attained 1 h after administration was 287 ng ml-1 (range 82-984). Heart rate and blood pressure did not change, but a significant increase (P less than 0.001) in PR (+12%), QRS (+13%) and QTc (+4%) duration occurred after drug administration. Flecainide was well tolerated. An idioventricular tachycardia was induced in one patient and two patients experienced side effects of the central nervous type: dizziness, blurring of vision and a sensation of warmth. In view of its activity flecainide appears to be a valuable addition to the antiarrhythmic armamentarium.
Adult↗
Current trends in transcatheter treatment of cardiac arrhythmias.
Catheter ablation has become established as a gold standard therapy for patients suffering from many supraventricular and ventricular arrhythmias, offering a curative alternative to these patients by way of destroying or isolating the arrhythmia substrate. Radiofrequency has been used as a primary source of energy for transcatheter ablation due to its safety and efficacy. Another technique is transcoronary chemical ablation, consisting of the infusion of ethanol through the coronary blood supply to the site of origin of the arrhythmia. Most supraventricular arrhythmias like atrial tachycardia, atrioventricular nodal reentrant tachycardia and arrhythmias related to atrioventricular accessory pathways can be managed with radiofrequency catheter ablation. However, some concerns exist regarding the value of this technique for the treatment of atrial flutter and ventricular tachycardia. In this review we discuss the state-of-the-art in catheter ablation of cardiac arrhythmias and its future perspectives.
Catheter Ablation↗