1,721,030 research outputs found
Polymorphous ventricular tachycardia as undesirable effect of the association of quinidine treatment with hysteresis ventricular inhibited pacing
No full textHolter monitoring in a 75-year-old man with a VVI pacemaker with rate hysteresis and concomitant quinidine treatment documented the occurrence of several episodes of non-sustained polymorphous ventricular tachycardia, triggered by each first paced beat following the longer escape interval. These arrhythmias disappeared when quinidine was withdrawn or when the pacemaker was reprogrammed without hysteresis. We hypothesize that the association of the different effects produced by hysteresis and quinidine created the electrophysiologic substrate for the observed arrhythmias
Effects of intracoronary administration of bradykinin on the impulse activity of afferent sympathetic unmyelinated fibers with left ventricular endings in the cat.
No full textIn anesthetized and artificially ventilated cats, we recorded the impulse activity of 23 afferent sympathetic unmyelinated fibers with left ventricular endings, dissected from the left sympathetic rami T3 and T4. All fibers displayed a spontaneous discharge at a rate of 0.79 +/- 0.2 (mean +/- SE) impulses/sec. During constriction of the thoracic aorta, the discharge increased to 1.92 +/- 0.2 impulses/sec. During myocardial ischemia, produced by interruption of left main coronary artery perfusion, supplied through an extracorporeal pump, the impulse activity increased to 1.73 +/- 0.3 impulses/sec. The mean latency for this excitation was 16.5 +/- 1.5 sec. The intracoronary administration of bradykinin (5 and 10 ng/kg) elicited a marked increase in impulse activity that, following 5 ng/kg, reached 2.06 +/- 0.2 impulses/sec, after a latency of 18 +/- 2 sec and in absence of significant hemodynamic changes. Myocardial ischemia and bradykinin never revealed the existence of silent afferent fibers included in the split nerve strand. The results obtained with this experimental model indicate that the ventricular endings of these afferent sympathetic unmyelinated fibers act as "polymodal" receptors. We hypothesize that the peripheral mechanism for cardiac nociception involves intensive excitation of fibers discharging spontaneously and not recruitment of silent fibers which are purely nociceptive in function
Patients with arrhytmogenic right ventricular cardiomyopathy remain at risk of sudden despite theraphy with beta-blockers and/or class III antiarrhythmic drugs
No full textAblazione transcatetere nei portatori di defibrillatore cardioverter affetti da tachicardia ventricolare incessante o iterativa
No full textDisparate unloading efficacy of the calcium channel blockers, verapamil and nifedipine, on the failing hypertensive left ventricle
No full textCalcium channel blockers reduce arterial smooth muscle tone and lower blood pressure. They may be regarded as left ventricular (LV) unloading agents. LV unloading efficacy of nifedipine (15 patients) and verapamil (14 patients) was tested in hypertensive decompensated patients, during a 1-month treatment period. Nifedipine persistently reduced systemic vascular resistance (SVR), mean arterial pressure, mean pulmonary wedge pressure (PWP), and LV diastolic diameter, and improved cardiac index and velocity of circumferential fiber shortening (Vcf). All of the patients had relief from dyspnea and reduction in heart size. The only side effect was ankle edema in six. Verapamil reduced SVR and mean arterial pressure and was not effective on PWP, LV diastolic diameter, and Vcf. The drug was discontinued in two patients who developed severe dyspnea at rest after 3 to 4 days of continuous oral treatment. Clinical symptoms and signs did not improve in the remaining patients despite persistent pressure reduction. A less potent vasodilating action of verapamil and a prominent depression in cardiac contractility may account for the differential results with the two compounds, in spite of a shared vasodilating antihypertensive effect. These findings indicate that functional changes in the failing hypertensive heart may differ from one calcium blocker to another as a result of interaction and relative preponderance of influence on afterload and contractility
L'ABLAZIONE CHIRURGICA SENZA CEC DELLE VIE ACCESSORIE LATERALI E POSTERIORI SINISTRE NELLA SINDROME DI WPW
No full textGlobal versus regional myocardial ischaemia: differences incardiovascular and sympathetic responses in cats
No full textThe cardiovascular and sympathetic responses to occlusions of the left main ("global" ischaemia) or distal left anterior descending ("regional" ischaemia) coronary artery were studied in 19 anaesthetised cats with chronic sinoaortic baroreceptor denervation. "Global" ischaemia, before vagotomy, resulted in a significant reduction of mean arterial pressure (MAP), left ventricular pressure (LVP), and LVdP/dtmax while sympathetic efferent impulse activity was significantly augmented during the initial 15 +/- 2 s of occlusion (early phase) and, vice versa inhibited during the subsequent 20 +/- 2 s of occlusion (late phase). Vagotomy did not modify the haemodynamic responses, however, a significant increase in sympathetic discharge was detectable during the whole occlusion period (early and late phases). "Regional" ischaemia, before vagotomy, resulted in a significant increase in sympathetic neural discharge and MAP, with no changes in left ventricular function. After vagotomy the occlusion elicited a significant increase in MAP, LVP, LVdP/dtmax and efferent sympathetic neural activity. These excitatory responses were abolished after the interruption of a large part of the cardiac sympathetic afferents. Thus coronary artery occlusion induced haemodynamic and sympathetic reflex responses that were dependent upon the interaction of opposite influences mediated by the simultaneous activation of cardiac vagal and sympathetic afferents. The extent of "ischaemic myocardium" represented a determinant factor for the prevailing type of neural response
Radiofrequency catheter ablation of incessant ventricular tachycardia in patients with implanted cardioverter-defibrillator
No full textModulation of the atrioventricular node conduction to achieve rate control in patients with atrial fibrillation: long-term results
No full textModulation of the AV node reduces the ventricular rate during AF, without affecting AV conduction during sinus rhythm. Acute and long-term results of AV node modulation in 75 patients with AF and severe related symptoms of heart failure are presented in this study. The procedure involved, in all cases, the selective ablation of the posterior inputs to the AV node; in a subgroup of 15 patients with poor modification of AV conduction properties, a sequential approach involving subsequent anterior input ablation was performed. The procedure caused acutely a prolongation of the Wenckebach cycle length (38 patients in sinus rhythm) from 334 +/- 88 to 470 +/- 80 ms (P 120 beats/min) that caused severe palpitations; these patients were considered as late clinical failures (8/75; 11%). All patients reported a substantial subjective improvement and an increased exercise tolerance, as documented by a semiquantitative questionnaire. There were no episodes of late AV block or sudden cardiac deaths. In conclusion, modulation of the AV node--either by slow pathway ablation, or by a "sequential" posterior and anterior approach in refractory patients--allows a long-term control of the ventricular rate and prevents the recurrence of severe clinical symptoms in more than 75% of patients with drug refractory AF
Cardiac rhythm in hypertension assessed through 24 hour ambulatory electrocardiographic monitoring. Effects of load manipulation with atenolol, verapamil, and nifedipine
No full textIn systemic hypertension left ventricular wall stress (afterload) is reduced and function enhanced, compared with normal, in the presence of concentric hypertrophy; the opposite occurs when hypertrophy is combined with dilatation. In this study we tested the hypothesis that cardiac rhythm may be related, in part, to the interacting variables: left ventricular structure, afterload, and function. Eighty-five primary hypertensives were divided into three groups: group 1 (24 cases with normal sized heart), group 2 (33 cases with concentric hypertrophy), and group 3 (28 cases with hypertrophy and dilatation). Cardiac rhythm, through 24-hour ambulatory electrocardiographic monitoring, and end-systolic left ventricular circumferential wall stress were investigated before and after seven days of treatment with atenolol, verapamil, and nifedipine in groups 1 and 2, and with the two calcium antagonists in group 3. Atrial and ventricular extrasystoles were recorded in 75 to 100% of the subjects in the control group (13 normotensives) and in the hypertensive groups. Average 24 hour atrial ventricular extrasystoles in group 1, and ventricular extrasystoles in group 2, were similar to normal before treatment and were not affected by drugs; changes in circumferential wall stress with treatment were comparable. In group 2 the number of atrial extrasystoles in 24 hours was significantly higher than in all the other groups. They were not influenced by changes in wall stress, and were interpreted as related to the atrial 'booster pump' action in the presence of concentric hypertrophy. In group 3 a great number of ventricular extrasystoles was associated with the highest baseline left ventricular afterload; circumferential wall stress and ventricular extrasystoles were poorly affected by verapamil, while the remarkable circumferential wall stress reduction caused by nifedipine was paralleled by an obvious decrease in ventricular extrasystoles. These data support the possibility that in systemic hypertension a relation exists between cardiac structure, load, and rhythm, and that ventricular arrhythmias may benefit from effective left ventricular unloading
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