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The incidence of secondary ventricular fibrillation (VF) complicating acute myocardial infarction (AMI) was 2.4% in a large cohort of unselected patients with AMI (142 of 5,839). Secondary VF was more frequent in patients with recurrent AMI (4%) than in those with a first AMI (1.9%) (p

We examined the role of chronic (greater than 1 month) angina pectoris (AP) before acute myocardial infarction (AMI) in predicting hospital and long-term mortality rates among 4166 patients with first AMIs. The prevalence of AP in these patients was 43%. Chronic AP was more common in women (49%), patients with hypertension (49%), and diabetic patients (49%) than in men and counterparts free of the former conditions (p less than 0.005). In patients with AP the hospital course was more complicated and non-Q-wave AMI was more common than in counterparts without AP. In-hospital (16%), as well as 1 (8%)- and 5-year postdischarge (26%), mortality rates in hospital survivors were higher among patients with previous AP than in patients without previous AP (12%, 6%, and 19%, respectively) (p less than 0.01). After adjustment for age and all other predictors of increased hospital mortality rates in this cohort of patients, AP preceding AMI emerged as an independent predictor of increased hospital mortality rates (odds ratio 1.30; 90% confidence interval 1.10 to 1.53). For postdischarge mortality rates (mean follow-up 5 1/2 years), the covariate-adjusted relative risk of death in patients with AP was similar at 1.29 (p less than 0.0001; 90% confidence interval 1.16 to 1.44), according to estimation by Cox proportional hazards model. These data support the notion that preexisting AP identifies a group of patients at increased risk of death.

Among 4,720 consecutive hospital survivors from acute myocardial infarction (AMI) treated in 13 coronary care units between July 1981 and August 1983, the estimated prevalence of electrocardiographic left ventricular (LV) hypertrophy was 6.1%. The prevalence of electrocardiographic LV hypertrophy increased with age and was higher in patients with previous myocardial infarction, angina and systemic hypertension. Mean age of patients with electrocardiographic LV hypertrophy was 67.2 vs 61.4 years in counterparts free of electrocardiographic LV hypertrophy. Patients with electrocardiographic LV hypertrophy had a higher rate of congestive heart failure on admission, or developing during their stay in coronary care units. The 1- and 5-year mortality rates were 19.7 and 46.6% among patients with electrocardiographic LV hypertrophy versus 8.7 and 26.2%, respectively (p less than 0.001) in patients without this finding. The covariate-adjusted odds ratio of 1-year mortality was 1.88 for the presence of electrocardiographic LV hypertrophy when age alone was adjusted for, and 1.51 (90% confidence interval, 1.09 to 2.10) when multiple covariate adjustment was undertaken. After multiple covariate adjustment for 5-year mortality after discharge, the relative risk associated with electrocardiographic LV hypertrophy was 1.51 (90% confidence interval, 1.26 to 1.80). The results of the present study showed that the presence of electrocardiographic LV hypertrophy on the discharge electrocardiogram of survivors from AMI is associated with a 1.5-fold increase of short- and long-term mortality. Patients with electrocardiographic LV hypertrophy, potentially at an increased post-discharge risk, may be candidates for early noninvasive testing and more intensive follow-up after recovering from AMI.

purpose: The purpose of this study was to report the incidence, the antecedents, and the clinical significance of clinically recognized cerebrovascular accidents or transient ischemic attacks (CVA-TIA) complicating acute myocardial infarction. patients and methods: During 1981 to 1983, a secondary prevention study with nifedipine (SPRINT) was conducted in 14 hospitals in Israel among 2,276 survivors of acute myocardial infarction. During the study, demographic, historical, and medical data were collected on special forms for all patients with diagnosed acute myocardial infarction in 13 of these 14 hospitals (the SPRINT registry, n=5,839). Mortality followup was completed for 99% of hospital survivors for a mean follow-up of 5.5 years (range: 4.5 to 7 years). results: The incidence of CVA-TIA was 0.9% (54 of 5,839). The latter rate increased significantly only with age, from 0.4% among patients up to 59 years old to 1.6% among those aged greater than or equal to 70 years. Multivariate analysis identified age, congestive heart failure, and history of stroke as predictors of CVA-TIA during the acute phase of myocardial infarction. Patients with CVA-TIA exhibited a complicated hospital course, with a 15-day mortality rate of 41%. Subsequent mortality rates in survivors at 1 and 5 years were 34% and 59%, respectively. Rates at the same time points in patients without CVA-TIA were 16%,11%, and 29% (p conclusion: In this large cohort of consecutive patients with myocardial infarction, CVATIA was a relatively infrequent complication of acute myocardial infarction. Factors independently favoring the occurrence of CVA-TIA were old age, previous CVA, and congestive heart failure. CVA-TIA occurring during acute myocardial infarction independently increased the risk of early death threefold as well as the risk of long-term mortality in early-phase survivors (2.5-fold).

The records of 483 patients admitted to the emergency room because of syncope were reviewed. Thirty seven patients (7.7%) were found to suffer from transient ischemic attack- (TIA) related syncope. This group is the subject of this report. Of these patients, 28 (76%) were men (mean age 71 years). Seven patients reported previous syncopal episodes. Past history revealed a high rate of ischemic heart disease (70%) and hypertension (68%). Concurrent neurologic symptoms, which led to the diagnosis of TIA-related syncope, included mainly vertebrobasilar symptoms: vertigo (in 55% of the patients), ataxia (46%), parasthesia (41%). Two patients most probably were presenting bilateral carotid artery disease. Various diagnostic tests (including electroencephalography, computed tomography, sonography, and cerebral angiography) were used to exclude other causes of syncope. During follow-up (mean 14.5 months) four patients (11%) had an additional episode of TIA and in three of them syncope reappeared. One patient had a complete stroke. We conclude that TIA is a much more frequent explanation for syncope than has been previously argued. These patients tend to be elderly males with high incidence of ischemic heart disease and hypertension. The concurrent neurologic symptoms, leading to the diagnosis, represent mainly vertebrobasilar territory ischemia.

Signal-averaged electrocardiograms were obtained in 53 consecutive patients with a first acute myocardial infarction (AMI) who survived the first 10 days of hospitalization. The recording was performed twice, at Day 1 and at Day 10 of hospitalization, in patients without bundle-branch block and who did not receive antiarrhythmic therapy. Signal-averaged ECGs were obtained with an instrument which analyzes the presence of late potentials (LP) in each individual precordial lead. There were 41 men and 12 women, mean age of 67 years. On Day 1, three patients had L.P (5.6%). On Day 10, LP was recorded in 11 patients (21%). In only one patient was LP transient. Patients who developed LP by Day 10 (absent in Day 1) had statistically significant lower root mean square (rms) voltage and higher QRS duration than patients who did not develop LP on Day 10. In conclusion, in patients with a first AMI who survive the initial hospitalization period and are not in need of antiarrhythmic therapy have an incidence of LP of 21%. A predischarge recording is preferable since this will maximize the chances of detecting LP.

Earlier studies have suggested that patients exhibiting late (> 24 h) ventricular fibrillation during acute myocardial infarction had a poorer outcome in comparison to myocardial infarction patients with early (< 24 h) ventricular fibrillation. Between August 1981 and July 1983, 5839 consecutive patients with acute myocardial infarction were hospitalized in 13 out of 21 operating coronary care units in Israel. Demographic and medical data were collected from hospitalization charts and during 1 year of follow-up. Mortality assessment was done for 99% of hospital survivors up to mid-1988 (mean, 5.5 years). The incidence of ventricular fibrillation in the SPRINT Registry was 6% (371/5839). Patients with ventricular fibrillation in the setting of cardiogenic shock (n = 107) were excluded from analysis. Patients with late ventricular fibrillation (n = 109; 41%) were older and had a more complicated hospital course than patients with early ventricular fibrillation (n = 155; 59%). In-hospital and 1-year post-discharge mortality were significantly higher in patients with late ventricular fibrillation (63% and 17%) as compared to patients with early ventricular fibrillation (26% and 4%, respectively; P < 0.05 for each). This difference vanished 5 years after hospital discharge. After multiple logistic regression analysis late occurrence of ventricular fibrillation emerged as an independent predictor of increased in-hospital mortality (Odds ratio, 4.29; 95% confidence interval, 2.11-8.74) but not for subsequent death. Patients with late ventricular fibrillation during the hospital course of acute myocardial infarction had a poorer immediate and subsequent outcome in comparison to patients with early ventricular fibrillation.

Controlled clinical trials have demonstrated the efficacy of reducing the blood levels of low-density lipoprotein cholesterol in reducing the incidence of coronary artery disease in hypercholesterolemic middle-aged men. However, a similar reversibility of the risk of coronary artery disease has not been demonstrated for high-density lipoprotein cholesterol elevation and triglyceride reduction. Therefore, the effect of administering 400 mg of bezafibrate retard daily versus placebo (double blind) to patients with myocardial infarction preceding randomization by 6 months to 5 years, or a clinically manifest anginal syndrome documented by objective evidence of dynamic myocardial ischemia, or both, is being investigated. Three thousand subjects (aged 45 to 74 years) are being enrolled from 19 cardiac departments in Israel, with total serum cholesterol between 180 and 250 mg/dl, high-density lipoprotein cholesterolor = 45 mg/dl and triglyceridesor = 300 mg/dl. In addition, low-density lipoprotein cholesterol concentrations are required to beor = 180 mg/dl (or = 160 mg/dl for patients aged50 years). Patients needing lipid-modifying therapy, exhibitingor = 1 prespecified exclusion criterion or not giving informed consent, or a combination, are not randomized. The primary end points for evaluating efficacy are the incidence of fatal and nonfatal myocardial infarction, and sudden death. The hypothesized effect of bezafibrate administration under the aforementioned protocol is to reduce an estimated cumulative end point event incidence ofor = 15% by 20 to 25% over an average follow-up period of 6.25 years, through early 1998, when the last patient recruited will have completed 5 years.(ABSTRACT TRUNCATED AT 250 WORDS)

Plasma viscosity, fibrinogen and haematocrit were measured in 80 patients with unstable angina on the 1st, 2nd and 5th day of hospitalization. In the group of patients who developed acute myocardial infarction (AMI) during hospitalization (20 patients), plasma viscosity was elevated during the entire observation period (1.69 +/- 0.05 cp, normal range 1.38-1.48 cp), while in patients who did not develop AMI, plasma viscosity was only mildly elevated (1.59 +/- 0.05 cp, P less than 0.001 vs the group who developed AMI) and tended to normalize towards the 5th day of hospitalization. Fibrinogen and haematocrit showed similar variations between the two groups. In a group of 20 patients who received heparin, the studied parameters were similar to the group who did not develop AMI. The importance of haemorheological factors in the clinical course of unstable angina is thus emphasized.

The purpose of this study was to determine the coronary angiographic correlations (specifically disease of the left anterior descending coronary artery) of reciprocal ST segment depression appearing during inferior acute myocardial infarction. Forty six patients (41 men and five women; mean age 56 years) were allocated into two groups based on the extent of precordial ST segment depression: widespread (V1-V6) ST depression v localised (V1-V4) ST depression. Patients with no reciprocal ST depression or patients with ST depression in V1-V4 but with ST elevation in V5 and V6 (inferolateral acute myocardial infarction) were excluded. All patients were catheterised during hospital admission for infarction. Twenty four of the 28 patients with ST depression in V1-V6 had significant lesions in the left anterior descending coronary artery whereas 16 of the 18 patients with ST depression in V1-V4 had insignificant or no lesions in the left anterior descending artery. The sensitivity, specificity, and positive and negative predictive values of widespread ST depression in predicting disease in the left anterior descending coronary artery were 92%, 80%, and 86% and 89% respectively. In patients with inferior acute myocardial infarction and precordial ST depression, the extent of ST depression is of clinical significance. Widespread (V1-V6) ST depression suggests disease of the left anterior descending coronary artery, whereas localised ST depression (V1-V4) indicates its absence.

A retrospective review of the records of 135 patients with proven or suspected endocarditis, seen between January 1970 and December 1987, is presented. Among the findings: (1) Mitral valve prolapse (MVP) as an underlying lesion was more common in the 1980s group of patients (22%) than in the 1970s group (6%, p less than 0.01); (2) no significant difference was found in the occurrence of pathogens between the 1970s and the 1980s groups of patients; (3) in most patients (17 of 19) with MVP, the organisms isolated were Streptococci viridans; (4) most patients (15 of 17) with MVP had undergone a dental procedure without prior antibiotic treatment in the two months prior to admission. Prophylactic antibiotic treatment is suggested in patients with MVP undergoing dental procedure, especially in a subset of patients with flail or redundant valve leaflet as 16 of our MVP patients (out of 17) had this pathology on echocardiogram.

The hospital records of 126 patients over 75 years of age with transmural myocardial infarction initially treated in the coronary care unit were compared with a concurrent similar group of 94 patients admitted directly to the general medical wards. The in-hospital mortality rate for both groups together was 40%. The mortality rate within the coronary care unit was 24% as compared with 46% in the ward group (P < 0.005). However, the mortality rate for the coronary care unit group as a whole (including those patients later transferred to the general ward) was 35 versus 46% in the ward group. Congestive heart failure and cardiogenic shock were the most frequent complications in both groups (47 and 30%, respectively), and they were the main cause of death. Patients with these complications were less likely to be successfully resuscitated, even in the coronary care unit. The overall incidence of serious ventricular arrhythmias and complete heart block was similar to that reported for younger patients. Eleven patients in the coronary care unit group were successfully resuscitated from these arrhythmias and eight survived to be discharged from hospital. In contrast, only two patients in the ward group were successfully resuscitated and eight (9%) patients died suddenly and the fatal event could not be diagnosed. We concluded that elderly patients with an acute myocardial infarction can benefit from early admission to a coronary care unit. J Am Geriatr Soc 35:915–919, 1987

We analyzed right ventricular (RV) regional wall motion by two-dimensional echocardiographic (2D echo) and multigated acquisition radionuclear (MUCA) studies in 104 patients with acute inferoposterior myocardial infarction (AIPMI). Sixty-eight patients (65 percent) had 2D echo RV regional wall motion abnormalities (RV dysfunction (RVD) group) while 36 patients showed no 2-D echo RV regional wall motion abnormalities (no-RVD group). The RVD group had a higher incidence of jugular venous engorgement (p

In this study of 14 patients hospitalized with a first event of myocardial infarction, maximal ST segment depression in precordial leads V2 and V3 was the sole ECG finding during chest pain in the first 24 hours of evolving posterolateral infarction, based upon further two-dimensional echocardiographic examination and cardionuclear imaging. Other ECG findings compatible with posterolateral infarction such as the appearance of Q waves in leads V5 and V6, increased R/S ratio in leads V1 and V2, and a diminution of R wave amplitude in leads 1, aVL, V5, and V6 were relatively delayed manifestations in the majority of patients. The clinical course of all patients was benign. It therefore seems reasonable to conclude that ST segment depression in leads V2 and V3 in the absence of reciprocal ECG changes may represent the initial ECG finding of posterolateral infarction in the suitable clinical context of an acute coronary event.

We tested the efficacy of intravenous amiodarone (5 mg/kg) in slowing ventricular response and/or restoring sinus rhythm in 26 patients with paroxysmal or new atrial fibrillation with fast ventricular response. There were 16 men and 10 women with ages ranging from 35 to 84 years, mean 63 years. Intravenous amiodarone initially slowed the ventricular response in all patients from 143 +/- 27 to 96 +/- 10 beats/min (P less than 0.001). Twelve patients (46%) reverted to sinus rhythm within the first 30 min (range 5 to 30 min, mean 14 +/- 9 min). One patient reverted to atrial flutter after 10 min and 40 min later to sinus rhythm. Six patients (23%) converted to sinus rhythm after 2 to 8 hr and in these 6 cases, the initial slowing in ventricular response obtained with amiodarone persisted until conversion. Seven patients (27%) did not convert to sinus rhythm following amiodarone administration and they required further medical therapy to slow the ventricular response and/or to convert to sinus rhythm. No serious side effects from drug administration were noted. Intravenous amiodarone appears as a highly effective medication in the conversion or control of new onset atrial fibrillation with fast ventricular response.

Based on two-dimensional echocardiographic wall motion abnormalities, 82 patients with acute inferior wall myocardial infarction were divided into 3 groups: group 1. predominant right ventricular infarction-20 patients; group 2. combined right and left ventricular infarction-33 patients; and group 3. predominant left ventricular infarction-29 patients. There were no significant statistical differences between the three groups regarding age, sex, Killip class on admission and jugular venous engorgement. Group 2 patients had higher peak creatine kinase levels and a lower rate of life threatening ventricular arrhythmia than the other groups. On M-mode echo, patients in group 1 had higher RV/LV ratios and lower left ventricular systolic and diastolic dimensions than group 3 patients. On 2-D echo and radionuclear studies, group 1 patients had more right ventricular wall motion abnormalities and minimal left ventricular wall motion disturbances. The left ventricular ejection fraction was higher and the right ventricular ejection fraction lower in group 1 patients than in those groups 2 and 3. The electrocardiogram showed small Q and relatively tall R waves in II, III, AVF in group 1 patients, and deep Q with loss of R waves in patients with combined or exclusive left ventricular infarction (groups 2 and 3). We conclude that predominant right ventricular infarction, which occurs in 24% of inferior wall infarction patients cannot be characterized clinically; however, an electrocardiographic pattern was found to detect this form of infarction with a sensitivity of 80% and a specificity of 70%. Combined left and right ventricular infarction and exclusive left ventricular infarction could be detected electrocardiographically with a sensitivity of 70% and a specificity of only 30%.

Eleven patients, three with acute anterior myocardial infarction and eight with anterior ischemia, who developed transient right axis deviation with a left posterior hemiblock pattern during the acute phase of myocardial infarction or ischemia are described (study group). A correlation between their electrocardiographic pattern and the angiographic findings was made. The arteriographie findings were compared with those of a group of 24 patients with acute anterior myocardial infarction or ischemia without transient right axis deviation (control group).The main electrocardiographic characteristics of the right axis deviation pattern were: 1) an average shift of the mean frontal axis to the right of 42° (10° to 94°); 2) increased voltage of R waves in leads II, HI and aVF and appearance of small Q waves or decreased voltage of Q waves if previously present in the same leads; 3) decreased voltage of R waves and appearance of deep S waves in lead aVL; and 4) inverted T waves and isoelectric ST segments in leads II, III and aVF.Coronary angiography revealed that the study group had a higher incidence of significant right coronary artery obstruction and collateral circulation between the left coronary system and the posterior descending artery than did the control group (100 versus 25% and 73 versus 0%, respectively; p < 0.01). There were no differences between the groups regarding left anterior descending and circumflex artery disease. Transient right axis deviation during anterior myocardial infarction or ischemia represents different degrees of left posterior hemiblock, which is probably a consequence of decreased blood supply to the left posterior fascicle and is highly correlated with the presence of significant right coronary artery stenosis and collateral circulation between the right and left coronary systems.

Summary Time course evolution of R, Q, T and ST components of the electrocardiogram during the first 12 hours of an acute myocardial infarction was studied. A comparison between anterior-extensive and anteroseptal wall infarctions (anterior group), and inferior-extensive and inferior wall infarction (inferior group) showed appearance of significant Q waves within two hours in both groups. R wave loss was nearly a mirror image of Q wave development in both groups. T waves became negative and ST more isoelectric earlier in the inferior than in the anterior group. When combined variations of the four electrocardiographic components were analyzed, four stages of acute infarction were delineated. Stage I-tall R, no Q, ST elevation and positive T; Stage II-significant Q wave appearance; Stage III-negativity of T waves; and Stage IV-ST isoelectric. The inferior group reached stages III–IV within 12 hours; the anterior group remained mostly in stage II. An early appearance of Q waves correlated well with rapid progression to stages III–IV within 12 hours in both infarction groups.

Ajmaline was administered intravenously to six patients with the Wolff-Parkinson-White syndrome for the acute management of paroxysmal atrial flutter (three patients) or fibrillation (three patients) with a fast ventricular response (over the accessory pathway). Ajmaline increased refractoriness in the accessory pathway in all three patients with atrial flutter and stopped the flutter in one. The drug completely abolished preexcitation in two of the three patients with atrial fibrillation, decreasing the means ventricular rate of 240 and 300 beats/min to 110 and 180 beats/min, respectively. In the third patient with atrial fibrillation, ajmaline increased refractoriness over the accessory pathway, decreasing the mean ventricular rate of 300 beats/min to 160 beats/min. In two patients ajmaline was continued as an intravenous maintenance infusion until sinus rhythm was restored. It is concluded that ajmaline is an effective drug for the acute management of atrial flutter or fibrillation with a fast ventricular response in patients with the Wolff-Parkinson-White syndrome.

ADP induced human platelet aggregation was shown to be accentuated when tested at 20-30 degrees C as increased sensitivity and as a greater change of optical density although second stage aggregation and the release reaction did not occur. This previously undescribed phenomenon is defined as room temperature ADP induced first stage hyperaggregation. Aggregation, which occurs under the above mentioned conditions with a quantity of ADP insufficient to maintain the aggregation (usually less than 1.5 micron), is reversible when the temperature is raised to 37 degrees C. After rewarming to these temperatures, second stage aggregation appeared in the presence of larger quantities of ADP (usually more than 2 microns) and could be blocked by aspirin. The absence of the release reaction was demonstrated with a lumi-aggregometer. Spontaneous cold induced platelet aggregation seen after chilling platelets to 0-4 degrees C is shown to be a distinct phenomenon.

The incidence, in-hospital evolution, and long-term follow-up were studied in patients who developed acute deviation of the mean (frontal) QRS axis to the right during an acute myocardial infarction (AMI). Among 3,160 patients evaluated, 13 (0.41 percent) developed left posterior hemiblock (LPHB) and 57 (1.8 percent) developed an incomplete form of LPHB, the right axis deviation group (RAD). Patients in the LPHB group had a statistically significant higher incidence of in-hospital morbidity (69 percent incidence of congestive heart failure) and mortality (38.5 percent). Follow-up revealed a statistically significant higher incidence of cardiac symptomatology (angina pectoris and congestive heart failure) in the RAD group than in the control group, mainly in patients in whom RAD persisted for more than 24 hours. Patients developing LPHB during AMI constitute a high risk population with a high incidence of morbidity and mortality. Patients developing RAD constitute an intermediate group (between the LPHB and the control group) characterized by a high incidence of cardiac symptoms at the time of follow-up.

Electrocardiographic assessment of the R/Q wave ratio (lead 2) of patients with a first acute inferior wall myocardial infarction (IWMI) offers important indirect quantitative information regarding the severity and extent of the myocardial damage. Eighty-eight consecutive patients with IWMI were investigated by echocardiography and radionuclear angiography. After measuring the R/Q ratio in lead 2 during the ST-wave stabilized stage of myocardial infarction, patients were separated into three groups--group 1 with an R/Q ratio greater than 2; group 2 with an R/Q ratio between 1 to 2; and group 3 with an R/Q ratio less than 1. Utilizing the information thus gathered from the electrocardiogram (ECG) offers a simple and efficient method for early prognosis which merits further investigation.

A 15-year-old boy who suffered from leg edema of unknown origin is described. The exclusion of any other cause for the edema, the clinical features, and the results of the dynamic tests performed suggested the diagnosis of "idiopathic edema," a syndrome described previously in women only. Spironolactone therapy brought about the disappearance of the edema and enabled the patient to return to his normal activities. This case report suggests that "idiopathic edema" is a syndrome common to both sexes, and is therefore not related to estrogen disturbances.

Amiodrone is a benytfuran derivative with class III anti arrhythmic effects. It has also been reported to convert atrial fibrillation and flutter to sinus rhythm and is highly effective for the prevention of atrial fibrillation (especially of the paroxysmal form) with an overall efficacy in the range of 70–50%. This high degree of efficacy was obtained in a majority of patients who had already failed various conventional anti arrhythmic agents. The mechanism of arrhythmia termination by intravenous amiodarone is not clear. The slowing in ventricular response, which most probably improves cardiac hemodynamics, has an indirect salutary effect. Despite the fact that none of the published reports on intravenous amiodarone used a placebo control group, these studies suggest that intravenous amiodarone has an important role in the acute treatment of atrial fibrilation with fast ventricular response.

Thirty-four cases of ventricular tachyarrhythmia characterized by polymorphy of the QRS complexes with changing R-R intervals and a heart rate of 150 to 300 beats/min, termed polymorphous ventricular tachycardia, are described. The factors involved in the appearance of this arrhythmia were the administration of antiarrhythmic drugs (quinidine 22 patients, procainamide 5 patients, ajmaline 1 patient), antianginal drugs (prenylamine [Synadrin] 4 patients) and antidepressant drugs (thioridazine 1 patient). Twenty-one patients were treated for premature ventricular complexes, three for chronic recurrent ventricular tachycardia, six for atrial flutter and fibrillation, three for anginal pain and one patient for mental depression. All patients except one had a drug-induced prolonged corrected Q-T interval before the appearance of polymorphous ventricular tachycardia. Most of the patients with this arrhythmia were considered to have severe myocardial disease. Lidocaine and electric cardioversion were administered to all patients, but were effective only in seven patients whose tachycardia occurred in short, single episodes. The most effective treatment (17 patients) was temporary ventricular pacing at rates ranging from 100 to 140 beats/min. Intravenous isoproterenol proved to be successful in another 10 cases. It is concluded that patients with severe myocardial involvement receiving antiarrhythmic drugs for premature ventricular complexes, especially the multiform variety, are at high risk for the development of polymorphous ventricular tachycardia.

A patient with clinically silent mitral valve prolapse experienced an episode of out-of-hospital cardiac arrest due to ventricular fibrillation. This arrhythmia was easily replicated in the electrophysiology laboratory and despite treatment with amiodarone alone and amiodarone in combination with propranolol. Amiodarone in combination with quinidine prevented the induction of ventricular fibrillation and proved effective during a 3-year follow-up period. Even though a clear-cut relationship between the arrhythmias and mitral valve prolapse cannot be established, this case suggests that sudden death can occur in patients with mitral valve prolapse but without the known risk factors for the development of sudden death.

The significance of dynamic changes of the QS wave magnitude, as demonstrated in the precordial leads, within the natural evolution of acute anterior wall myocardial infarction (AAMI) was assessed in 25 patients within two weeks of their admission to the intensive cardiac care unit. Two sets of tests, including 12-lead electrocardiogram and a full radionuclear study, were performed in two time periods: (1) within the first 48 hours of admission; and (2) between the 12th and 15th day after admission. Comparison and correlation between the electrocardiographic data, QS waves in leads V2 and V3 and in V1 to V6 (sigma QV2-3 and sigma QV1-6), and radionuclear regional ejection fractions of the noninfarcted posterior muscle (inferior, infero-apical, and posterolateral regions and posterior index) were done. Significant linear correlations were demonstrated between the electrocardiographic variant differences in percentages (sigma QV2-3 and sigma QV1-6) and the radionuclear variant differences, especially the posterolateral and the infero-apical regions, as well as the posterior radionuclear index (r between 0.5 and 0.75; p less than 0.01). In addition, almost all of the patients who showed deepening of QS waves in the precordial leads also showed an increase in regional ejection fractions in uninvolved myocardium, and vice versa. It is concluded that the dynamic changes of the QS wave magnitude in the precordial leads within the evolution of acute anterior myocardial infarction well reflect the changes of the posterior noninfarcted muscle contraction and therefore offers a simple, inexpensive, and indirect electrocardiographic method for evaluating changes in contraction patterns of noninfarcted myocardium.

Five patients with acute myocardial infarction had ventricular fibrillation as a complication of indicated temporary pacing. All five patients had evidence of right ventricular infarction (three patients with postmortem confirmation). The presence of right ventricular infarction seems to be a contributing mechanism involved in the induction of ventricular fibrillation during temporary pacing for bradyarrhythmia complicating acute myocardial infarction.

Forty patients with recurrent syncopal episodes of uncertain etiology were evaluated with a 60-degree head-up tilt table test for 60 minutes. There were 21 men and 19 women, with a mean age of 36 ± 19 years, a mean of 7.6 syncopal episodes per patient, and a mean duration of symptoms of 4.2 ± 6 years. Twelve patients had evidence of organic heart disease. Ten control subjects with no history of syncope were studied similarly. Syncope did not occur in any of these controls. Syncope occurred in 15 patients (37.5%) after a mean standing time of 42 ± 12 minutes. Syncope was due to a typical vasovagal reaction in 11 patients and to hyperventilation in three patients. One last patient fainted without changes in heart rate or blood pressure. In each case, symptoms during the test resembled those prevlously experienced.

Plasma viscosity and haematocrit were determined in 44 patients with acute myocardial infarction on the 1st, 2nd, 3rd and 10th day of hospitalization. The highest haematocrit value for the entire group was found on the 1st day of acute myocardial infarction--43.3 SD +/- 4.6% declining progressively to 38.8 SD +/- 3.5% on the 10th day (P less than 0.001). Plasma viscosity for the entire group was normal on the first day of acute myocardial infarction (1.44 SD +/- 0.10 cp) and started to increase on the second day (1.51 SD +/- 0.16 cp, P less than 0.001). A relationship was found between reinfarction or death (17 patients) occurring during hospitalization and changes in haematocrit and plasma viscosity. In this group plasma viscosity rose to 1.63 SD +/- 0.19 cp on the second day of acute myocardial infarction (P less than 0.001 vs plasma viscosity value on the first day). This elevation persisted on the third day. Haematocrit values in this group were 47.9 SD +/- 3.6% on the first day of acute myocardial infarction declining progressively and significantly afterwards. In the remaining patients both plasma viscosity and haematocrit were normal and did not change. No correlation of plasma viscosity and haematocrit were found when tested for other clinical complications, sex, age, maximal creatine phosphokinase values and coronary risk factors. We suggest that variations in haematocrit and plasma viscosity during acute myocardial infarction exist in a group of patients in whom reinfarction or death occurs. The changes in haematocrit and plasma viscosity precede the complications by 4-8 days.(ABSTRACT TRUNCATED AT 250 WORDS)

We report on twelve patients with alternating Wenckebach periods (AWP) occurring during an acute inferior myocardial infarction (AIMI). There were nine males and three females, with a mean age of 61 years (range, 43 to 75). AWP appeared during the first 48 hours of the AIMI in 10 patients and on the fourth day of hospitalization in two patients. AWP occurred spontaneously in nine patients and following the administration of atropine in the remaining three patients. Mean systolic blood pressure significantly decreased during AWP as compared to the period preceding or following the bradyarrhythmia (93 +/- 42 mmHg vs 123 +/- 37 mmHg, p less than 0.02). Killip functional class was significantly higher during AWP as compared to the period preceding or following the bradyarrhythmia (2.1 +/- 1.2 vs 1.5 +/- 0.8, p less than 0.02). Pacemaker therapy was initiated prophylactically in two patients, because of syncope in six, because of hemodynamic deterioration in two, and for syncope and hemodynamic deterioration in two. Three patients died in cardiogenic shock despite pacemaker therapy. No evidence of right ventricular infarction was seen in the patients. Atropine administration during AWP significantly increased the sinus rate and significantly decreased the ventricular rates and the systolic blood pressure. In addition, three patients developed long bouts of paroxysmal AV block. Isoproterenol administration improved AV conduction in one patient, caused no change in two patients and induced non-sustained ventricular tachycardia in three patients. In conclusion, AWP occurring during AIMI is a symptomatic bradyarrhythmia associated with hemodynamic deterioration.(ABSTRACT TRUNCATED AT 250 WORDS)

Summary The purpose of this study was to investigate the correlation between the origin of premature ventricular contractions (PVC's) appearing during acute myocardial infarction (AMI) and the location of the infarction as determined by the electrocardiogram (ECG). The PVCs were termed acute or chronic according to the time of their appearance. The origin of the PVCs, located at the left ventricle (anterior or posterior wall) or the right ventricle, was determined by ECG criteria. In 82 out of 91 cases of acute PVCs (90.2%), the PVCs presented an origin similar to the AMI location (p≤.001). In 23 cases with chronic PVCs, this correlation was not observed. In all 13 cases of primary ventricular fibrillation in which the PVCs origin was determined prior to the event, the PVCs were acute coming from the same location as the AMI. The effectiveness of lidocaine treatment on PVCs was also determined. Out of 44 cases with acute PVCs, 38 responded to lidocaine, with 37 of them showing an origin similar to the AMI location (p≤.001); 5 non-responders showed an origin different from the AMI location. No response was observed in 20 out of 23 cases with chronic PVCs. These results show a good correlation between the origin of the acute PVCs and the location of the AMI. It is concluded that the determination of the origin of PVCs appearing during AMI provides further clinical information as to the location of AMI, its prognosis in relation to serious arrhythmias and the resistance of certain PVCs to lidocaine treatment.

SummaryIn order to verify whether leukocyte aggregation correlated with aggregation of other cellular elements during inflammation, we examined the state of leukocyte adhesiveness/aggregation (LAA) in the peripheral blood and red cell aggregation. Correlation was found to be significant as was the correlation between LA A and fibrinogen, and with the fibrin/fibrinogen degradation products concentration during various inflammatory states. In vitro leukocyte aggregation was decreased when the cells were suspended in autologous heat defibrinogenated plasma as compared to cells suspended in autologous native plasma. Heat aggregated fibrinogen but not native fibrinogen caused leukocyte aggregation in vitro. Finally, Arvin defibrinogenation in rabbits reduced the state of LAA in endotoxinemic rabbits. Integrating all this information, we assume that fibrinogen participates not only in the aggregation phenomena of red cells and platelets, but also in those of leukocytes.

Two distinct electrocardiographic patterns of ventricular fibrillation (VF) complicating acute myocardial infarction (AMI) were observed in 34 patients during the first 24 hours from initial symptoms. Type 1 (seven patients) was characterized by fast disorganized ventricular activity, small voltage, and no clear identifiable QRS complexes (fine VF). Type 2 (27 patients) was defined as multiform QRS configuration (>300/min) with marked changes in the amplitude (polymorphous VF). Type 1 rhythm was seen mostly during the hyperacute ischemic phase, probably associated with total coronary vessel occlusion; type 2 was observed when Q waves were already present in the electrocardiogram.

We have reviewed all available noninvasive diagnostic studies for the evaluation of syncope of suspected cardiovascular origin. This eight-step diagnostic approach covers the majority of available syncopal etiologies. In patients evaluated for syncope, we believe a complete noninvasive evaluation should be performed (if clinically indicated) before performing invasive electrophysiologic studies.

Eighteen patients with a first AMI, who during the acute ischemic phase did not develop ST segment elevation, but only positive or peaked T waves, are described. Patients who do not develop ST segment elevation during evolving anterior AMI represent a subgroup with a high probability of total obstruction of the LAD artery with retrograde filling via collateral vessels and a small degree of left ventricular dysfunction. We assume that during the period of total obstruction there was preexisting adequate collateral circulation in order to prevent transmural ischemia, which explains the absence of ST segment elevation.

Echocardiographic evaluation of 42 patients with sarcoidosis disclosed 13 patients (group A) with abnormalities compatible with sarcoid heart involvement such as thickening or thinning of the septum (eight patients), pericardial effusion (four patients), and increased end-diastolic dimension of the left ventricle with decreased systolic function (three patients). The remaining 29 patients (group B) were diagnosed as having normal echocardiograms. The clinical data revealed no statistically significant difference between the groups regarding age, sex, chest x-ray stage, activity, and previous heart disease. Group A patients had older clinical onset of the disease (52 vs 83 months; p less than 0.05) and higher incidence of ECG abnormalities than group B patients. There were no statistically significant differences between the groups regarding two-dimensional echocardiographic internal dimensions of both ventricular chambers. The radionuclear right ventricular ejection fraction was low in both groups and the left ventricular ejection fraction was depressed in group A patients (p less than 0.01). As observed in pathologic studies, the septum is a target structure which can be characterized echocardiographically. Screening suspected sarcoid heart disease involvement is important to characterize patients with a relatively high risk of clinical cardiac abnormalities such as complete atrioventricular block, ventricular arrhythmias, congestive heart failure, and sudden death.

Four cases of longitudinal dissociation of the atrioventricular node, with dual pathways developing during the acute phase of an inferior wall myocardial infarction (three cases) or during acute ischemia (one case), are presented. In all four cases, two grossly different P-R intervals were recorded, and in two cases, studies of the His bundle confirmed the location of the dissociation within the atrioventricular node. In one case, premature atrial depolarization caused a bidirectional shifting of P-R intervals, while in the remaining three cases, premature ventricular depolarization (spontaneous or pacemaker-induced) was responsible for this phenomenon. In all cases, evidence of longitudinal dissociation of the atrioventricular node appeared during the acute phase of the infarction or ischemia, and in all of them the phenomenon was transient. This favors the assumption that this phenomenon is of a functional nature, most probably related to the ischemic lesion of the atrioventricular node.

The effect of glucagon on arrhythmias produced by digitalis (ouabain) and on ventricular automaticity was studied in 36 dogs. Glucagon abolished the arrhythmias in 26 dogs (72 percent), primarily by producing a sinus tachycardia with 1:1 ventricular response, thereby competing with and suppressing the ectopic rhythm. After administration of glucagon in the normal heart, ventricular automaticity was generally unchanged. During digitalis toxicity, glucagon had either not changed or decreased ventricular automaticity, the decrement in ventricular automaticity showing poor correlation with this agent's antiarrhythmic effect. Glucagon also induced an immediate rise, then a fall in serum potassium levels. It is concluded that a multiplicity of factors—enhanced automaticity of the sinoatrial node, improved atrioventricular conduction, changes in potassium levels and, at times, slight lowering of ventricular automaticity—all contribute to the antiarrhythmic capabilities of glucagon.

Of 139 consecutive patients with a first inferior acute myocardial infarction, 26 (19%) had advanced atrioventricular (AV) block and 113 (81%) did not. All were evaluated by 2-dimensional echocardiography (2-D echo) and radionuclide angiography. Patients with advanced AV block had lower radionuclide left ventricular (LV) ejection fraction (51 +/- 10 vs 58 +/- 11%, p less than 0.01), higher LV wall motion score on 2-D echo (5.6 +/- 2.6 vs 3.1 +/- 2.7, p less than 0.001), lower radionuclide right ventricular (RV) ejection fraction (32 +/- 15 vs 39 +/- 16%, p less than 0.001) and higher RV wall motion score on 2-D echo (3.4 +/- 1.7 vs 1.5 +/- 2, p less than 0.002) than did patients without AV block. The incidence rate of RV dysfunction was higher in patients with advanced AV block (78 vs 40%, p less than 0.02), and the mortality rate was also higher (although not significantly) in patients with advanced AV block (15 vs 6%). In conclusion, patients with inferior acute myocardial infarction and advanced AV block have larger infarct sizes (as seen on radionuclide angiography and 2-D echo) and lower RV and LV function than patients without AV block. This finding may explain the higher mortality rate observed in this group.

Thirty-two patients with LAF were studied. Nineteen (59 percent) were male subjects. Mean age was 46.8 years. They were followed up for 2 to 16 years. On admission, most patients (94 percent) were symptomatic and had palpitations, nine had nonspecific chest pain, and five had syncope or near syncope. Left atrial size measured by echocardiography was less than 40 mm in all patients. During the follow-up period, only one patient had a complication, ie, cerebral embolism. We conclude that LAF may be regarded as a relatively benign form of AF. According to our study, one of its features is left atrial size not larger than 40 mm in echocardiography.

A 52-year-old man had longstanding hypertension and asymemtric septal hypertrophy and normal major coronary arteries. His acute anterior wall ischemia gave rise to transient Q waves and septoapical dyskinesia, complicated by mural thrombus formation. Follow-up revealed a gradual and complete recovery of echocardiographic left ventricular function with total disappearance of mural thrombi and of electrocardiographic Q waves. Acute myocardial ischemia can cause prolonged electrical and mechanical stunning which can lead to mural thrombus formation.

A 27-year-old trained athlete with recurrent syncope of suspected vaso-vagal origin was evaluated. A 60 degrees head-up tilt table test reproducibly triggered the patient's spontaneous symptoms and allowed the investigation of different modalities of therapy (medical and pacing) in preventing syncopal episodes. The head-up tilt table test may be a useful tool in the evaluation of syncope of vaso-vagal origin, helping to determine the initial precipitating vagal event and the effect of therapy.

Elevated serum lactic dehydrogenase (LDH) levels, 595 to 615 microns/ml (normal less than 225 microns/ml) with predominance of LDH isoenzymes 2 and 3 was the early and only sign of occult malignant lymphoma in three patients. In the first patient, overt lymphoma appeared clinically only 2 months after the finding of elevated serum LDH levels, whereas in the other two asymptomatic patients, pathologic LDH levels were the only clues to the need for further diagnostic investigation. It is concluded that LDH may have a diagnostic value in the preclinical stage of malignant lymphoma. Thus, a patient with no apparent cause for elevated serum LDH levels warrants a thorough work-up including abdominal CT scan and even explorative laparotomy.

A total of 1744 patients admitted to the ICCU with acute myocardial infarction (AMI) were studied in 1462 consecutive days (1982-1986). The aim of the study was to check whether the localization of the AMI was time related. Anterior (anterolateral) (AW) (n = 834) versus inferior-posterior (inferolateral) (IPW) (n = 823) AMI were compared: a third group with isolated lateral wall (LW) AMI (n = 87) was included in the study. Significant differences between monthly AMI localizations were registered, but no rhythmicity (monthly, seasonal) was found. A small absolute prevalence of AW localizations was found in all four seasons, but monthly differences made those differences not statistically significant. Some significant correlation (p less than 0.01) was found between AW AMI domination and daily geomagnetic activity (GMA level I-IV). Only on days with low (quiet) levels of GMA were there more IPW AMIs. Adverse relationship was seen with LW AMI, relatively benign in AMI, was adversely correlated with GMA level (p less than 0.01). Differences in AW/IPW and left/right coronary artery autonomic receptors distribution and flow regulation and/or changes in cardiovascular homeostasis/coagulation, aggregation, viscosity, microcirculation, and so on connected with AMI expansion may be involved in these differences of AMI localization.

Nine patients are presented who had polymorphous ventricular tachycardia (PMVT) occurring during atrioventricular (AV) block. There were five men and four women with a mean age of 80 +/- 9 years. Five patients had organic heart disease and the remaining four had primary conduction disease (bundle branch block). AV block was complete in four patients (2:1 in three, and paroxysmal in two). The mean ventricular cycle length (of the AV block rhythm) was 1567 +/- 203 ms. The mean QT interval was 0.64 +/- 0.09 s and the mean QTc was 0.51 +/- 0.06 s. When compared to a similar control group with AV block but without PMVT, the ventricular cycle length was similar but the QT and QTc were significantly longer. PMVT was usually of short duration (eight beats to 12 s) and in seven of these nine patients, frequent premature ventricular beats (PVBs) were recorded at various times from the occurrence of PMVT. This is in contrast to the control patients in whom PVBs were detected in one patient only. In conclusion, patients with AV block who develop PMVT usually have longer QT intervals and have detectable PVBs on routine ECGs, unlike similar patients with AV block but without PMVT. In a patient with AV block, a QT interval above 0.60 s and PVBs on the ECG seem to indicate an increased risk for the development of PMVT.

The effect of intravenous (IV) amiodarone (300 mg) on heart rate was investigated in 22 patients with acute myocardial infarction (18) or ischemia (4) and sinus tachycardia. There were 11 men and 11 women (age range, 48 to 83 years; mean, 63.5). Amiodarone IV slowed the mean heart rate from 109 +/- 14 beats/min to 94 +/- 15 beats/min (p less than 0.0005). There was a linear correlation between the initial heart rate (preamiodarone) and the final heart rate (postamiodarone), (r = 0.6930, p less than 0.0005). Most of the patients with initial heart rates higher than the mean maintained relatively high heart rates (above the mean), while most patients with lower initial heart rates showed low heart rates (below the mean) after amiodarone administration. Patients in Killip class 1 showed a significant reduction in heart rate after receiving amiodarone, from a mean of 105 +/- 10 to 88 +/- 11 beats/min (p less than 0.01). Patients in Killip class 2 also had reduced heart rates (118 +/- 14 to 81 +/- 39 beats/min), but these changes were not statistically significant. Of the three patients in Killip class 3 to 4, the heart rate slowed by 10 beats/min in one, while in the remaining two no changes were observed. There were no significant side effects from the administration of amiodarone.