Coronary arterial spasm.
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Biomedical subjects
Publications and source records attributed to B Befeler.
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A 41-year-old man with a surgically closed atrial septal defect presented with anginalike symptoms of 5 years duration. While undergoing coronary arteriorgraphy, the patient sustained ventricular fibrillation which was converted successfully to sinus rhythm by a chest thump. This is the first reported case of such conversion. The mechanism of mechanical conversion from ventricular tachycardia, or fibrillation, to sinus rhythm may be that the mechanical stimulus interrupts a re-entry pathway or depresses ectopic impulses to allow the normal sinoatrial rhythm to emerge.
Programmed stimulation was alternatively performed exclusively from the right ventricular endocardium, exclusively from the left ventricular epicardium and simultaneously from both ventricles in 8 patients who did not have coronary artery disease or bundle branch block. A specially constructed QRS triggered pacemaker, (with a refractory period of 260 msec and an escape interval of 800 msec) connected to the right ventricular and left ventricular electrodes, was used to perform simultaneous biventricular stimulation. The latter had no untoward effects and was not more dangerous than exclusive right ventricular, or exclusive left ventricular, stimulation. In 3 patients, pacemaker-induced repetitive firing occurred during right and left ventricular pacing. Persistence of this phenomenon (in these 3 patients) during simultaneous biventricular stimulation is in keeping either with a microreentry occurring in the vicinity of the electrodes or with a macroreentry involving the bundle branches. A more precise evaluation of the reentry circuit requires that left ventricular pacing be performed from an endocardial (rather than from an epicardial) site. This study suggests that the pulse generator described in the present communication can be used to produce simultaneous atrial and ventricular activation (or pacing) by connecting one pole to an atrial electrode and the other pole to a ventricular electrode. This modality of stimulation can be effective in preventing or abolishing some types of reciprocating atrioventricular tachycardias.
Electrocardiographic (ECG) changes after left ventricular aneurysmectomy were analyzed in 20 patients, thirteen of whom had additional aorto coronary saphenous vein bypass surgery. ECG changes were correlated with postoperative clinical and hemodynamic results. Out of 14 patients (Group I) who showed hemodynamic and/or clinical improvement, eight had decrease of chronic ST segment elevation that was associated in five with loss of pathologic Q waves. In the remaining six patients (Group II) who showed no hemodynamic or clinical improvement as well as in six patients in Group I, chronic ST segment elevation persisted or increased and in some, new pathologic Q waves developed after surgery. The study suggests that loss of pathologic Q waves and/or decrease of chronic ST segment elevation in patients who undergo a left ventricular aneurysmectomy with aorto coronary saphenous vein bypass surgery may reflect postoperative clinical, hemodynamic and angiographic improvement. On the other hand, failure of these ECG changes to occur or, conversely, increased ST segment elevation and/or appearance of new Q waves may have no predictive value. The mechanisms for these ECG changes are discussed.
Eleven patients were studied and a total of 144 Wenckebach cycles in the AV node and 118 Wenckebach cycles in the His-Purkinje system were analysed to determine the incidence of typical and atypical Wenckebach periodicity, with particular emphasis on one variant of atypical Wenckebach that may simulate a Mobitz type II block. This pseudo-Mobitz II pattern was defined as a long Wenckebach cycle in which, at least, the last three beats of the cycle show relatively constant PR intervals (variation of no more than 0.02 s in surface leads and no more than 10 ms in His bundle electrograms) and in which the PR interval immediately following the blocked beat is shorter than the PR interval before the block by 0.04 s or more. Atypical Wenckebach cycles were found to be more common than the typical variety at both the AV node (67%) and His-Purkinje system (69%). The pseudo-Mobitz II pattern was seen in 19 per cent of atypical AV nodal Wenckebach periods and in 17 per cent of atypical His-Purkinje system Wenckebach cycles. The need to discern a 'classical' Mobitz II block from a pseudo-Mobitz II pattern, especially in the setting of an acute inferior myocardial infarction, is emphasised.
This report presents the experience obtained with the use of mechanical stimulation of the heart by external ("chest thump") and internal (stimulation via catheter) means in the treatment of tachyarrhythmias. The chest thump was used primarily for termination of ventricular tachyarrhythmias. Endocardial stimulation of the right and left ventricles and right atrium via catheters was used for both ventricular and supraventricular arrhythmias. The experience reported includes 68 patients, 19 of whom were treated successfully with mechanical stimulation and 49 of whom required other types of treatment. Of the 32 patients with 33 episodes of atrial tachycardia, eight episodes (24%) were treated successfully (three episodes by right atiral stimulation and five by right ventricular stimulation). Of the four patients with five episodes of junctional tachycardia, three episodes (60%) were treated successfully (one episode by right atrial stimulation and two by right ventricular stimulation). Of the 32 patients with ventricular tachycardia who experienced 37 episodes, 15 episodes (41%) were treated successfully (three by right ventricular stimulation, two by left ventricular stimulation, and ten by chest thump). In two of these patients, the thump was applied to an area of paradoxical pulsation.
Coronary artery aneurysms were found in 16 men between 37 and 62 years of age, mean 51 years. Aneurysms were of two types: saccular and fusiform. They involved the right coronary artery in 13 (87 per cent), the circumflex artery in eight (50 per cent) and the left anterior descending artery in five (31 per cent). In some patients, more than one vessel was involved. Twelve patients presented with angina pectoris, three with congestive heart failure and one with both. Five were in functional class II, eight were in class III and three were in class IV at the beginning of the study. The electrocardiogram showed evidence of previous myocardial infarction in four patients; four patients had left ventricular hypertrophy, one had left axis deviation, one had left bundle branch block, one had right bundle branch block, two had first degree atrioventricular block and seven had abnormalities in the S-T segment and T wave. Obstructive coronary disease was present in all; the obstruction score was from 1 to 4 in three patients, from 5 to 9 in four patients and from 10 to 14 in the remaining nine. Similar aneurysms were found in the pulmonary artery of one patient and in the abdominal aorta of three patients; in seven of 14 patients with adequate venous angiograms, varicosities of the coronary venous tree were observed. Left ventricular dysfunction and angina pectoris were noted in patients with significant obstructive coronary disease (greater than 70 per cent) and also in patients without obstruction but with coronary aneurysms. Ten patients were treated surgically; nine underwent aortocoronary bypass and one mitral valve replacement. Criteria for bypass was the presence of obstructive disease and medically unresponsive angina pectoris. All but one surgically treated patient showed improvement. The functional class in medically treated patients was unchanged. Fourteen patients were still alive at the completion of the study. The findings of this study suggest that angina pectoris and left ventricular dysfunction can occur with coronary artery aneurysm without coronary artery obstructions. Coronary aneurysms may be a subset of atherosclerosis, and this process may involve other vascular territories. The prognosis in those patients appears to be no worse than in patients with obstructive coronary disease and no aneurysms.
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His bundle recordings were performed in 2 patients in whom AV nodal bypass tracts coexisted with intermittent AV conduction disturbances occurring below the site from which the His bundle deflection was recorded. Case 1 had: (a) tachycardia dependent right bundle-branch block, (b) persistent HV prolongation, and (c) bradycardia dependent AV block. Case 2 showed: (a) intra-atrial conduction delay, (b) tachcardia dependent left bundle-branch block with HV prolongation, (c) bradycardia dependent HV conduction disturbance, (d) tachycardia-bradycardia syndrome of an unusual type; the latter presumably resulted, during atrial flutter, from the alternation of rapid AH conduction through the bypass tract with intermittent (complete) distal His bundle block or bilateral bundle-branch block.
A 43-year-old man who had undergone aortocoronary saphenous vein bypass developed disruption of the proximal aorto-saphenous vein anastomosis. Although rare, a mediastinal hematoma secondary to leakage or disruption of an anastomotic site should be considered in patients who develop a mediastinal mass after aortocoronary bypass surgery.
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Late clinical and hemodynamic evaluations in 18 patients with ventricular aneurysmectomy and aorta-coronary bypass are presented. Tne patients had significant obstructive lesions in two major vessels (55 per cent), and 6 had extensive three vessel disease (33 per cent). In 13 patients, 21 aorta-coronary saphenous bypass grafts were performed in addition to aneurysmectomy. The operative mortality rate was 11 per cent. One patient died suddenly 5 months after the operation (one year mortality rate 17 per cent). The 15 surviving patients have been followed up for 12 to 41 months (average 24 months). Clinical results were considered excellent in 2 patients who have been asymptomatic (Class I, N.Y.H.A.). Nine others were considered to have good clinical results (Class II). Five patients have continued to have congestive heart failure and angina on minimal effort (Class III or IV). Six of the 11 patients considered to have excellent or good results underwent postoperative hemodynamic studies 6 to 34 months after the operation. A significant increase in cardiac index was documented in all 6 patients. Paradoxic movement was not detected in any of the postoperative ventriculograms. Five of the seven venous grafts inserted were patent. Elevated left ventricular end-diastolic pressure (LVEDP), low cardiac index, and a persistent dyskinetic area in the left ventricle were found in 2 patients considered to have poor clinical results. Clinical and hemodynamic evaluations have shown a significant improvement in most patients surviving ventricular aneurysmectomy. However, postoperative systemic embolism, myocardial infarction, progression of coronary artery disease, transient cerebral ischemic attacks, graft occlusion, arrhythmias, and mitral regurgitation in previously prolapsed mitral valve leaflets account for progressive disability and limited activity after a successful operation.
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The relationship between systemic and renal hemodynamics was studied in 20 patients with advanced cirrhosis of the liver. Cardiac output was assessed by an indicator dilution technique, and both mean renal blood flow and intrarenal blood flow distribution were determined by the 133Xe washout method. Ten patients had elevated cardiac outputs (7.14 to 13.58 L/min; HCO group), seven patients had normal cardiac ouptputs (5.16 to 6.78; NCO group), and three had low cardiac outputs (3.65 to 4.1; LCO group). Renal hemodynamics did not correlate with cardiac output (r = 0.051; N.S.), since comparable reductions in mean renal blood flow occurred in both the LCO and HCO patients. Similarly, the degree of cortical ischemia, as assessed by percentage flow to the rapid flow component (C1%), did not correlate with cardiac output (r = 0.007; N.S.). Vasomotor instability as assessed by intrapatient variability of sequential xenon washout studies occurred frequently, and its magnitude did not correlate with cardiac output (r = -0.069; N.S.). These studies demonstrate that the abnormalities of intrarenal blood flow in cirrhosis are independent of alterations in cardiac output. Furthermore, the finding of marked intrarenal hemodynamic instability in the majority of patients with cirrhosis suggests that caution should be exercised in interpreting studies assessing the efficacy of vasoactive agents on renal hemodynamics in this disease, since the changes attributed to treatment may merely reflect spontaneous change.
The conditions associated with prolapse of the posterior leaflet of the mitral valve are multiple. The mechanisms of mitral valve prolapse as well as the pathogenesis of pain and ectopic impulse formation are reviewed. Propranolol appears to be the drug of choice for the symptomatic treatment of patients with this syndrome since it decreases myocardial oxygen demand and wall tension thus reducing or abolishing the discrepancy between myocardial oxygen demand and supply within the mitral apparatus. It has also been reported to modify the auscultatory findings associated with this condition. The frequency of this mitral valve abnormality in patients with obstructive coronary artery disease is reviewed. It appears that prolapse of the posterior leaflet scallops in patients with significant obstructive coronary artery disease represents an intermediate stage before mitral insufficiency occurs. This group of patients with papillary muscle dysfunction includes those with prolapsed leaflets without mitral insufficiency, those with systolic murmurs and compensated heart failure and others with progressive cardiac decompensation and severe mitral regurgitation.
His bundle recordings and premature atrial stimulation from coronary sinus, mid-right atrium and high-right atrium were performed in a patient with repetitive supraventricular tachycardias. Regardless of the paced site, there was a range of coupling intervals during which testing stimuli elicited short runs of premature beats. The corresponding P waves were positive in leads I, II and III and had a high-to-low right atrial activation sequence. Their morphology was similar to that of sinus beats. However, sustained tachycardia occurred only when pacing was performed from the coronary sinus. Therefore, it is postulated that the site of stimulation might be important in the genesis and (perhaps) perpetuation of this arrhythmia by changing the site and (or) mode of entry into the area where this type of tachycardia occurs. Though sinus node reentry was the most likely mechanism, it could not be determined whether the circuit involved the sinus node per se or the so called perinodal fibers.