[Cardiac arrhythmia: terminology update].
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Biomedical subjects
Publications and source records attributed to M Z Berisso.
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BACKGROUND: Programmed ventricular stimulation performed early after acute myocardial infarction allows to identify patients at risk of sudden death and sustained ventricular tachycardia with high degree of predictive accuracy. This procedure, however, because of its invasive nature, is not desirable as a screening test for large numbers of patients. Therefore, it should be performed on a smaller group of postinfarction patients preselected on the basis of noninvasive testing. The aim of the present study was to identify, early after acute myocardial infarction, any procedure among noninvasive testing, able to selected with the highest sensitivity patients at risk of sudden death and sustained ventricular tachycardia to submit to programmed ventricular stimulation. METHODS: Two hundred and sixty four consecutive patients with recent myocardial infarction were evaluated and followed during a period of 12 months. In each patient 48 epidemiological, clinical and laboratory variables were evaluated. Laboratory variables were acquired between the 7th and the 12th day after the acute event. RESULTS: Multiple linear regression analysis showed that only Killip class, the number of ventricular premature depolarizations per hour and the presence of ventricular late potentials were significantly and independently related to the occurrence of sudden death and sustained ventricular tachycardia (F = 18.7; p < 0.00001). Combinations of these variables, determined at cut off levels best discriminating two subgroups of patients at different risk of the end-point events, proved to be able to accurately predict the outcome of our patients. The presence of at least one of the following conditions: Killip class > or = 2, ventricular premature depolarizations > or = 30 per hour, ventricular late potentials allowed to identify a first subgroup of patients at risk with a sensitivity of 100% (p = 0.00007), whereas the presence, at the same time, of all the above mentioned parameters allowed to identify a second subgroup of patients at risk with a 44% of positive predictive value (p = 0.00007). CONCLUSIONS: Our findings suggest that the first subgroup of postinfarction patients selected on the basis of noninvasive testing should undergo programmed ventricular stimulation, the second might be treated by adequate antiarrhythmic therapy without undergo any further investigation, whereas the remaining patients (without late potentials, in Killip class 1 and with ventricular premature depolarizations < 30 per hour) might be discharged without any antiarrhythmic therapy.
Clinical significance, short and long-term prognostic value, and treatment of supraventricular tachyarrhythmias were evaluated in 208 patients with definite acute myocardial infarction (AMI). No patient received thrombolytic therapy. In Coronary Care Unit supraventricular tachyarrhythmias were detected by continuous electrocardiographic monitoring in 30 (14%) patients: 18 had atrial fibrillation, 1 atrial flutter, 9 paroxysmal atrial tachycardia and 2 non-paroxysmal junctional tachycardia. These episodes began within the first 48 hours of AMI in 93% of patients, and generally they were preceded by frequent or repetitive atrial premature beats. Supraventricular tachyarrhythmias were significantly associated with older age, higher incidence of overt left ventricular dysfunction (both p less than 0.05) and higher Peel Index (p less than 0.02). They caused severe hemodynamic consequences in 20% of patients. In 8 patients they were selflimiting, in 20 they were suppressed by means of medical therapy and in one by DC countershock. During hospitalization supraventricular tachyarrhythmias recurred in one patient; moreover, in this period cardiac death occurred in 26% of patients with supraventricular tachyarrhythmias and in 13% of the remaining (p: ns). Multivariate analysis showed that supraventricular tachyarrhythmias are not important factors in identifying patients at risk of cardiac death. At hospital discharge, patients with supraventricular tachyarrhythmias showed significantly higher values of left ventricular end-diastolic and end-systolic dimensions (both less than 0.05), and a greater use of digitalis-diuretics and/or vasodilators (p less than 0.03). By contrast, in patients with and without supraventricular tachyarrhythmias no significant difference was present with regard to the frequency of New York Heart Association functional classes III-IV for congestive heart failure, frequency of significant tachyarrhythmic events during 24-hour continuous electrocardiographic recording, X-ray cardiac size and left ventricular ejection fraction at rest. In the 2 years following AMI, survival curves showed no significant difference in the risk of cardiac death among patients with or without supraventricular tachyarrhythmias; in particular, in the first group only 2 patients had severe hemodynamic events and no patient showed recurrences of tachyarrhythmia. Our findings suggest that although supraventricular tachyarrhythmias complicating AMI frequently occur in patients with severe cardiac disease they are not related to a higher risk of cardiac death either during in-hospital period or in the 2 years following AMI; medical therapy is effective and safe to suppress these arrhythmias; a systematic use of specific antiarrhythmic drugs to prevent their recurrences is not necessary.
Hypertrophic cardiomyopathy has been investigated mainly at referral institutions. Thus, the clinical history of the disease that emerges from published studies could be influenced by a bias in patient selection. In the present study, we compared the clinical features of an outpatient population of 25 patients who had hypertrophic cardiomyopathy with those reported in 78 studies published during the past five years. In the 25 study patients, age, sex, and the extent of left ventricular hypertrophy, as well as the prevalence of diastolic filling abnormalities, subaortic obstruction, and ventricular arrhythmias, were similar to those in patients described in the literature. Cardiac symptoms, however, were much less severe in the study patients. Eighteen patients (72 percent) were asymptomatic, six (24 percent) had mild symptoms, and only one (4 percent) had moderate-to-severe symptoms. Of 24 patients followed for a mean period of 4.4 years (range, 2.9 to 5.7), none died or had clinical deterioration. Of 3404 patients described in the 78 studies we reviewed, 2483 (73 percent) came from only two referral institutions. Of the 1721 patients in whom severity of symptoms was reported, 757 (44 percent) had moderate-to-severe symptoms. However, 727 (96 percent) of these patients were studied at one of the same two referral institutions. We conclude that the natural history of hypertrophic cardiomyopathy may be more benign than can be inferred from published reports.
We report a case of early pace-maker malfunction associated with a collection of air which separates the anodal contact plate of a unipolar permanent generator from the underlying tissues. The air pocket resulted from a complication of the percutaneous technique used to introduce the electrocatheter through the subclavian vein. Loss of capture was attributed to a critical increase in impedance to current flow in the pacing system. The malfunction was corrected by simple non-invasive procedures at the patient's bedside. Air pocket can cause the loss of stimulation of the pace-maker.
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The effect of cimetidine on the cardiovascular system of normal subjects has been assessed. Eight healthy subjects were submitted to i.v. infusion on 200 mg of cimetidine in 2'; at a second stage, five of these were treated with placebo in equal volume and infusion speed. Polygraphic (LVET, PEP, PEP/LVET, triple product) and echocardiographic (systolic volume, cardiac capacity, velocity, circumferential shortening and ejection fraction) parameters were considered and heart frequency and arterial pressure measured. Measurements were carried out prior to infusion and for periods subsequent to the end of infusion. The results showed a statistically significant reduction only in heart frequency, triple product and cardiac output of subjects treated with cimetidine; no modifications were observed in subjects treated with placebo. It is concluded that cimetidine changes in heart frequency and its related parameters.