The cardiovascular effects of morphine. The peripheral capacitance and resistance vessels in human subjects.

To evaluate the effects of morphine on the peripheral venous and arterial beds, 69 normal subjects were evaluated before and after the intravenous administration of 15 mg morphine. Venous tone was determined by three independent techniques in 22 subjects. The venous pressure measured in a hand vein during temporary circulatory arrest (isolated hand vein technique) fell from 20.2+/-1.4 to 13.4+/-0.9 mm Hg (P < 0.01) 10 min after morphine, indicating that a significant venodilation had occurred. With the acute occlusion technique, morphine induced a reduction in forearm venous tone from 12.8+/-1.1 to 7.9+/-2.3 mm Hg/ml/100 ml (P < 0.01). Although forearm venous volume at a pressure of 30 mm Hg (VV[30]) was increased from 2.26+/-0.17 to 2.55+/-0.26 ml/100 ml, measured by the equilibration technique, the change was not significant (P > 0.1). Of note is that the initial reaction to morphine was a pronounced venoconstriction, demonstrated during the first 1-2 min after the drug. (Isolated hand vein pressure increased to 37.2+/-5.4 mm Hg, P < 0.01). This rapidly subsided, and by 5 min a venodilation was evident. Morphine did not attenuate the venoconstrictor response to a single deep breath, mental arithmetic, or the application of ice to the forehead when measured by either the isolated hand vein technique or the equilibration technique. To evaluate the effects of morphine on the peripheral resistance vessels in 47 normal subjects, forearm blood flow was measured plethysmographically before and 10-15 min after the intravenous administration of 15 mg of morphine. Although mean systemic arterial pressure was unchanged, forearm blood flow increased from 2.92+/-0.28 to 3.96+/-0.46 ml/min/100 ml (P < 0.01), and calculated vascular resistance fell from 42.4+/-5.2 to 31.6+/-3.2 mm Hg/ml/min/100 ml (P < 0.01). When subjects were tilted to the 45 degrees head-up position, morphine did not block the increase in total peripheral vascular resistance that occurs; however, it did significantly attenuate the forearm arteriolar constrictor response (before morphine, + 25.7+/-5.4; after morphine, + 13.7+/-5.3 mm Hg/ml/min/100 ml, P < 0.05). However, morphine did not block the post-Valsalva overshoot of blood pressure, nor did it block the increase in forearm vascular resistance produced by the application of ice to the forehead. Similarly, morphine did not block the arteriolar or venoconstrictor effects of intra-arterially administered norepinephrine. Morphine infused into the brachial artery in doses up to 200 mug/min produced no changes in ipsilateral forearm VV[30], forearm blood flow, or calculated forearm resistance. Intra-arterial promethazine, atropine, and propranolol did not block the forearm arteriolar dilator response to intravenous morphine; however, intra-arterial phentolamine abolished the response. These data suggest that in human subjects, morphine induces a peripheral venous and arteriolar dilation by a reflex reduction in sympathetic alpha adrenergic tone. Morphine does not appear to act as a peripheral alpha adrenergic blocking agent but seems to attenuate the sympathetic efferent discharge at a central nervous system level.

Effect of propranolol in patients with myocardial infarction and ventricular arrhythmia.

The Beta-Blocker Heart Attack Trial was a placebo-controlled, randomized, double-blind clinical trial of the long-term administration of propranolol hydrochloride to patients who had had at least one myocardial infarction. Among 3,837 patients followed up for an average of 25 months, 3,290 (85.7%) had 24 hour ambulatory electrocardiograms performed at the baseline examination. Four classifications of arrhythmia were examined. One of these, the presence of complex ventricular arrhythmias (at least 10 ventricular premature beats/h, or at least one pair or run of ventricular premature beats or multiform ventricular premature beats) was the subgroup of major interest. Regardless of the classification, the presence of arrhythmia identifies a group of patients with a higher risk of total mortality, coronary heart disease mortality, sudden cardiac death and instantaneous cardiac death. The a priori subgroup hypothesis that sudden death would be preferentially reduced by propranolol in patients with complex ventricular arrhythmias was not supported. The relative benefit of propranolol in reducing sudden death for this subgroup was 28 versus 16% for the subgroup without ventricular arrhythmia (relative risk of 0.72 versus 0.84, a nonsignificant relative difference of 14%). There were similar findings for two of the three other classifications of arrhythmia and for the other response variables. Although propranolol does not appear to be of special relative benefit in patients with ventricular arrhythmia, the presence of the arrhythmia does identify a high-risk group. The mechanism by which propranolol reduces mortality is still unclear, but is probably not solely an antiarrhythmic one.

Differential risk patterns associated with 3 month as compared with 3 to 12 month mortality and reinfarction after non-Q wave myocardial infarction. The Diltiazem Reinfarction Study Group.

Follow-up data for 515 survivors of acute non-Q wave myocardial infarction were categorized according to mortality: 1) between hospital discharge and 3 months after infarction (early), and 2) between 3 and 12 months after infarction (late). The mortality rate decreased steadily for the first 3 months and was constant thereafter. There were 25 early and 32 late deaths. After adjustment for the longer time associated with the 3 to 12 month period, the relative risk per unit time of early as compared with late mortality was 2.64. Risk factors for early mortality were different from those that predicted late mortality. Independent predictors of mortality between hospital discharge to 3 months after infarction were ST segment depression that persisted during hospitalization (p less than 0.0001), in-hospital reinfarction (p = 0.0006) and a history of congestive heart failure (p = 0.0255). Persistent ST depression and in-hospital reinfarction had neither a univariate nor an independent association with 3 to 12 month mortality. Age (p less than 0.0001), reinfarction between discharge and 3 months (p = 0.0147) and diabetes (p = 0.0404) were independently associated with late mortality. Early mortality was only 0.5% (1 of 199) in patients with no ST depression at either baseline or discharge (group 1); 4.8% (8 of 168) in those with ST depression at exactly one time point (group 2) and 13.7% (16 of 117) in those who had ST depression present at both time points (group 3). All pairwise differences were significant (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Events in the cardiac arrhythmia suppression trial: baseline predictors of mortality in placebo-treated patients.

Patients randomized to placebo in the encainide and flecainide arms of the Cardiac Arrhythmia Suppression Trial (CAST) have been found to have a relatively low 1-year mortality rate of 3.9% in comparison with previous studies of patients in the postmyocardial infarction period. To determine the comparability of CAST with previous studies, baseline variables were examined in the 743 patients randomized to placebo in the flecainide and encainide arms of CAST. Twenty-three baseline characteristics were correlated with major outcome events: arrhythmic death (16 events), total mortality (26 events) and congestive heart failure (51 events). On multivariate analysis the risk of new or worsening congestive heart failure was significantly associated with diuretic use, diabetes, high New York Heart Association functional class, age, prolonged QRS duration and low ejection fraction. The risk of arrhythmic death or resuscitated cardiac arrest was significantly associated with an index Q wave myocardial infarction, history of heart failure, use of digitalis, diabetes and prolonged QRS duration. Total mortality or resuscitated cardiac arrest was significantly associated with an index Q wave myocardial infarction, diabetes, ST segment depression, high functional class, prolonged QRS duration and low ejection fraction. The variables at baseline associated with mortality from all causes or arrhythmic death or resuscitated cardiac arrest and heart failure in the CAST placebo-treated patients are similar to those identified in previous postmyocardial infarction studies. Thus, the observation of increased mortality in CAST associated with the administration of encainide and flecainide for suppression of ventricular premature depolarizations is probably applicable to any comparably defined group of patients in the postmyocardial infarction period.

Prognostic significance of ventricular premature depolarizations measured 1 year after myocardial infarction in patients with early postinfarction asymptomatic ventricular arrhythmia.

OBJECTIVES: The objective of this study was to examine the relation between death and the frequency of premature ventricular depolarizations measured approximately 1 year after myocardial infarction. BACKGROUND: The reported association between premature ventricular depolarizations and death in the weeks after myocardial infarction is in part the basis for the use of antiarrhythmic drugs. Such an association has not been reported on for observations obtained at a much greater interval after myocardial infarction. METHODS: We examined the association between mortality and premature ventricular depolarization rates measured 1 year after myocardial infarction in patients with asymptomatic ventricular arrhythmia early (between 6 and 90 days, median 28) after infarction, as measured by 24-h ambulatory electrocardiographic recording. The study group consisted of 502 patients enrolled in the Cardiac Arrhythmia Pilot Study during 1983 to 1985. They were followed up during the course of the study and subsequently by a National Death Index search (average follow-up interval 1,080 days). RESULTS: Death was recorded for 87 patients through 1987. Because patients were admitted to the Cardiac Arrhythmia Pilot Study only if they had greater than or equal to 10 ventricular premature depolarizations/h, the arrhythmia rate measured at baseline (that is, early after infarction) was not expected to, and did not, predict mortality. In 360 patients ventricular premature depolarization rates were measured approximately 1 year from their index myocardial infarction while they were not receiving antiarrhythmic therapy. In these patients, who had survived 1 year after the index infarction, the rate of ventricular premature depolarizations/h measured 1 year after infarction was highly predictive of subsequent death (p less than 0.001). Recent heart failure and a history of diabetes mellitus were also strongly predictive of death. CONCLUSION: The prognostic value of ventricular premature depolarizations observed 1 year after a myocardial infarction may be significant even in a sample selected for frequent ventricular premature depolarizations observed early after the event.

Free fatty acids and arrhythmias following acute coronary artery occlusion in pigs.

The arrhythmogenic potential of elevated serum free fatty acids (FFA) was investigated in closed-chest pigs following acute coronary artery occlusion. Animals both with and without ventricular irritability before the FFA rise were studied. No significant increase in PVC frequency occurred and only 1 out of 17 animals developed ventricular fibrillation in the 60 min following acute FFA elevation. In this situation, FFA did not significantly influence the appearance of arrhythmias.

Failure of hyaluronidase to alter the early course of acute myocardial infarction in pigs.

The effect of hyaluronidase on the early course of acute myocardial infarction was evaluated in closed chest anesthetized pigs. One hour after balloon catheter occlusion of the left anterior descending coronary artery, hyaluronidase (500 units/kg body weight) was rapidly infused in 10 animals while 9 received no treatment. The animals were than observed over the next 4 hours. Cardiac output, heart rate, mean arterial pressure and left atrial pressure were not significantly affected by treatment. Heart rate increased and arterial pressure decreased in each group to a comparable degree of 5 hours, but left atrial pressure and cardiac output were unaffected. Precordial S-T segment mapping revealed no significant difference between the two groups. S-T segments rose to a comparable degree in each group and peaked before 1 hour. Hyaluronidase had no acute effects on the S-T segment map in the first 30 minutes after infusion or during the subsequent return of the map toward control level. Slightly lower S-T segments in the hyaluronidase-treated group at 5 hours was of borderline significance but was attributed to factors other than the drug intervention. Changes in ventricular wall motion were assessed angiographically, and all animals manifested akinetic or dyskinetic segments. A significant reduction in shortening fraction of involved segments was seen after occlusion, but no difference was observed between the two groups at 5 hours. Shortening fraction of the combined anterior and anteropical segments decreased from 66 +/- 10 to 20 +/- 6 percent at 5 hours in the hyaluronidase group (no. = 7) whereas in the control group (no. = 6) it decreased from 68 +/- 6 to 28 +/- 9 percent. Comparable increases in end-diastolic volume were also present at 5 hours in each group. Volumes increased from 80.6 +/- 5.1 to 97.5 +/- 6.4 ml3 at 5 hours (P less than 0.05) in the hyaluronidase-treated group (no. = 10) compared with 86.9 +/- 8.9 to 104.8 +/- 11.0 ml3 (P less than 0.05) in the control group (no. = 8). Hyaluronidase did not alter the early course of acute myocardial infarction in pigs. Species differences may contribute to different results reported to date.

Electrocardiographic evolution of posterior acute myocardial infarction: importance of early precordial ST-segment depression.

Precordial ST-segment depression is typically observed in anterior non-Q-wave acute myocardial infarction (AMI), and is generally not regarded as an indication for acute thrombolytic therapy. Of 544 patients with creatine kinase (CK)-MB-confirmed non-Q-wave AMI randomized to the prospective multicenter Diltiazem Reinfarction Study, 50 patients (9.2%) had isolated precordial ST-segment depression of 1 mm or more in 2 or more contiguous precordial electrocardiographic leads (V1-V4). Serial electrocardiograms recorded at study entry (mean 50.5 hours after onset of chest pain), on study day 2, study day 3 and at predischarge showed that in 23 of 50 patients (40%) electrocardiographic evidence of posterior AMI evolved, defined as an R wave of 0.04 second or more in lead V1 and an R:S greater than or equal to 1 in lead V2. In 18 of these 23 patients (78%), posterior AMI had evolved by study day 3, and none had an abnormal reelevation of CK-MB (every 12-hour sampling) for up to 14 days of hospitalization. Compared with the remaining 27 patients who had electrocardiographic features of anterior non-Q-wave AMI only, the 23 with initial precordial ST segment depression in whom posterior AMI developed had significantly higher mean peak CK values (1,051 +/- 172 vs 663 +/- 89 IU, p less than 0.009) and greater mean precordial ST-segment depression in lead V1 (0.28 vs + 0.19 mm, p = 0.01), in lead V2 (1.3 vs 0.26 mm, p = 0.003) and in lead V3 (2.0 vs 0.93 mm, p = 0.0004).(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical significance and prognostic importance of left ventricular hypertrophy in non-Q-wave acute myocardial infarction.

Left ventricular (LV) hypertrophy is known to be an independent risk factor for cardiac death, but its significance in non-Q-wave acute myocardial infarction (AMI) has not been assessed previously. In a randomized diltiazem-placebo-controlled therapeutic trial of non-Q-wave AMI confirmed by creatine kinase-MB (CK-MB), 126 of 544 patients (23%) exhibited LV hypertrophy using standard voltage criteria. Compared to patients without LV hypertrophy, patients with LV hypertrophy were significantly older (65 vs 60 years, p less than 0.0001) and had smaller peak adjusted CK levels (490 +/- 376 vs 666 +/- 726 IU/liter, p less than 0.001) than patients without LV hypertrophy. Patients with and without LV hypertrophy did not differ significantly in acute mortality during hospitalization, progression to Q waves, reinfarction by CK-MB criteria or angina associated with transient electrocardiographic changes. Compared with patients without LV hypertrophy, those patients with non-Q-wave AMI and LV hypertrophy had a 2-fold higher incidence of reinfarction (24 vs 12%, p less than 0.005) and death (19 vs 9%, p = 0.044) during the first year of follow-up. Multivariate regression analysis revealed that the relative risk of death and reinfarction during the initial year after AMI was increased by a factor of 1.7 and 2.1 among patients with LV hypertrophy, respectively. It was therefore concluded that, although patients with LV hypertrophy and non-Q-wave AMI have smaller enzymatic infarcts and the same short-term prognosis as do patients without LV hypertrophy, their reinfarction and mortality rates are significantly increased during the first year of follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)

Congestive heart failure after acute myocardial infarction in patients receiving antiarrhythmic agents for ventricular premature complexes (Cardiac Arrhythmia Pilot Study).

The Cardiac Arrhythmia Pilot Study (CAPS) was a randomized, double-blind trial of antiarrhythmic drugs (encainide, flecainide, moricizine, imipramine and placebo) in 502 patients with an ejection fraction greater than 0.20 and at least 10 ventricular premature complexes/hour, 6 to 60 days after acute myocardial infarction. Patients were followed for 1 year and the incidence of new or worsened congestive heart failure (CHF) was evaluated. Heart failure in the 1-year follow-up was gauged by the development (in order of increasing severity) of new symptoms (grade 1), the need for a change in therapy, including addition of digitalis, addition or increase of dose of diuretics or afterload reduction agents or discontinuation of beta-blocking agents (grade 2), or by hospitalization (grade 3). Sixty-one of 502 patients (12%) required hospitalization for CHF in the 1-year follow-up. One hundred five of 403 patients (26%) in the active treatment group and 18 of 99 patients (18%) in the placebo group (difference not significant) developed CHF requiring hospitalization or a change in therapy or both. Although patients with severely impaired ejection fraction were excluded, new or worsened CHF was common in follow-up during CAPS.

Biobehavioral variables and mortality or cardiac arrest in the Cardiac Arrhythmia Pilot Study (CAPS).

The frequency of ventricular premature complexes and the degree of impairment of left ventricular ejection fraction are major predictors of cardiac mortality and sudden death in the year after acute myocardial infarction. Recent studies have implicated psychosocial factors, including depression, the interaction of social isolation and life stress, and type A-B behavior pattern, as predictors of cardiac events, controlling for known parameters of disease severity. However, results tend not to be consistent and are sometimes contradictory. The present investigation was designed to test the predictive association between biobehavioral factors and clinical cardiac events. This evaluation occurred in the context of a prospective clinical trial, the Cardiac Arrhythmia Pilot Study (CAPS). Five-hundred two patients were recruited with greater than or equal to 10 ventricular premature complexes/hour or greater than or equal to 5 episodes of nonsustained ventricular tachycardia, recorded 6 to 60 days after a myocardial infarction. Baseline behavioral studies, conducted in approximately 66% of patients, included psychosocial questionnaires of anxiety, depression, social desirability and support, and type A-B behavior pattern. In addition, blood pressure and pulse rate reactivity to a portable videogame was assessed. The primary outcome was scored on the basis of mortality or cardiac arrest. Results indicated that the type B behavior pattern, higher levels of depression and lower pulse rate reactivity to challenge were significant risk factors for death or cardiac arrest, after adjusting statistically for a set of known clinical predictors of disease severity. The implication of these results for future research relating behavioral factors to cardiac endpoints is discussed.

Frequency and significance of late evolution of Q waves in patients with initial non-Q-wave acute myocardial infarction. Diltiazem Reinfarction Study Group.

Serial 12-lead electrocardiogram and plasma creatine kinase (CK)-MB values from 544 patients with confirmed non-Q-wave acute myocardial infarction (AMI) were analyzed to define the rate of progression of non-Q-wave AMI to Q-wave AMI and to examine its relation to CK-MB evidence of extension. The baseline electrocardiogram was obtained 50 +/- 10 hours after AMI and compared with subsequent electrocardiograms at 48 and 72 hours after baseline record and at discharge. Plasma CK-MB was assayed every 12 hours after baseline. A total of 76 patients (14%) progressed to Q-wave AMI. Compared to the 468 patients who retained non-Q-wave AMI, those patients who evolved Q-wave AMI were more likely to exhibit ST elevation greater than or equal to 1.0 mm in greater than or equal to 2 infarct-related leads (49 vs 32%, p less than 0.005), higher peak CK values with the index AMI (754 +/- 625 vs 611 +/- 604 IU; p = 0.0018) and a greater incidence of CK-MB-confirmed extensions (18.5 vs 5.5%, p less than 0.0001). For those patients progressing to Q-wave AMI within 48 hours of baseline electrocardiogram, CK-MB extension occurred in 9.5% (4 of 42) versus 29.4% (10 of 34) of those who progressed after 48 hours (p = 0.0262). A distinct minority (14%) of patients with non-Q-wave AMI will develop Q waves before discharge. The progression to Q-wave AMI after initial non-Q-wave AMI appears to involve 2 different mechanisms: temporal lag in the electrocardiogram, and actual extension by quantitative CK-MB criteria.

Assessment of quality of life as observed from the baseline data of the Studies of Left Ventricular Dysfunction (SOLVD) trial quality-of-life substudy.

The improvement of aspects of a patient's quality of life may be as important as prolonging survival in evaluating clinical trials of heart failure. The purpose of this study was to analyze the psychometric properties of the baseline measures from the quality-of-life substudy from the Studies of Left Ventricular Dysfunction (SOLVD) trial. The measures included the 6-Minute Walk Test, Dyspnea Scale, Living with Heart Failure, Physical Limitations, Psychologic Distress and Health Perceptions, as reported by both patients and staff. Cognitive functioning, such as Vocabulary, Digit Span and Trails Making, was also assessed. Patients were classified as New York Heart Association class I (n = 158) versus II or III (n = 150). The internal consistencies (i.e., reliabilities) of the self-report measures were high, except for the Health Perceptions of Class II or III patients. Reliability of the SOLVD quality-of-life battery was confirmed by significantly better life quality among New York Heart Association class I patients versus class II or III patients combined on the Walk Test, Physical Limitations, Dyspnea, Living with Heart Failure, Psychologic Distress and staff perceptions of patient health. In accordance with prior studies, the measures were uncorrelated with left ventricular ejection fraction. By demonstrating strong internal consistencies, reliability based on physician reports, and independence of ejection fraction levels, use of this quality-of-life assessment battery in this and other clinical trials of compromised ventricular functioning is supported.

Relation of psychosocial and stress reactivity variables to ventricular arrhythmias in the Cardiac Arrhythmia Pilot Study (CAPS).

Both animal and human data implicate psychosocial distress and cardiovascular reactivity in response to challenge in the etiology of sudden cardiac death. In this study, the relation of these biobehaviorial factors to frequency of ventricular premature complexes, a predictor of sudden death was investigated. The study population was made up of patients enrolled in the National Heart, Lung, and Blood Institute's Cardiac Arrhythmia Pilot Study (CAPS). Ventricular premature complexes (VPCs) were assessed by multiple, 24-hour ambulatory electrocardiographic recordings. Patients completed trait psychosocial measures assessed at baseline and state psychosocial measures assessed periodically during a 1-year follow-up period. Psychosocial measures included self-reports of depression, anxiety, anger and type A behavior pattern. A competitive challenge using a video game was used as a stressor to elicit cardiovascular reactivity and was administered at baseline and during follow-up sessions. Cardiovascular reactivity was defined as peak level during stressor exposure minus the mean of resting levels for systolic and diastolic blood pressure and pulse rate. Results indicated that biobehavioral factors were not associated with diurnal VPC rates. Furthermore, biobehavioral factors did not predict response to antiarrhythmic therapy. Based upon the results of this study, it is speculated that the established relation between behavioral factors and sudden death may not be mediated by VPC rates.

Classification of deaths after myocardial infarction as arrhythmic or nonarrhythmic (the Cardiac Arrhythmia Pilot Study).

The Cardiac Arrhythmia Pilot Study (CAPS) was a randomized, double-blind trial of antiarrhythmic drugs (encainide, flecainide, moricizine, imipramine and placebo) in 502 patients with at least 10 ventricular premature complexes/hour, 6 to 60 days after acute myocardial infarction. CAPS tested the feasibility of performing a larger study to determine if suppression of ventricular ectopic activity after acute myocardial infarction could improve survival. Patients in CAPS were followed for 1 year. All death or cardiac arrest events were evaluated by at least 2 investigators using a classification scheme that characterized the underlying mechanism as cardiac arrhythmic, cardiac nonarrhythmic or noncardiac. Forty-five patients (9%) died or had cardiac arrest during the 1-year follow-up, 29 (64%) within 1 hour from the onset of symptoms and 16 greater than 1 hour from the onset of symptoms. Twenty-three deaths (51%) were classified as arrhythmic, 19 (42%) as nonarrhythmic and 3 (7%) as noncardiac. Acute myocardial ischemia or infarction was associated with the death/cardiac arrest event in 16 patients (36%), 8 in the arrhythmic death group. Discrepancies in classification among reviewers were particularly common in patients with long-standing symptoms of congestive heart failure, in whom it was frequently difficult to identify the precise moment of the onset of symptoms in the death/cardiac arrest event. Using only the temporal relation of symptoms to categorize deaths or cardiac arrests, the mechanism of 12 (27%) of the 45 patients was in disagreement with the classification based on the Events Committee review. Classification of death as sudden or nonsudden is not equivalent to the classification of death as arrhythmic or nonarrhythmic.

Evaluation of skeletal muscle capillary basement membrane thickness in congestive heart failure.

Although it has been demonstrated that during isotonic grip exercise patients with chronic congestive heart failure have an abnormally reduced forearm oxygen consumption resulting from a depressed forearm flood flow, there may be additional etiologies of this abnormality. To explore this possibility biopsies of the pronator teres muscle were taken in eight control subjects with normal cardiac hemodynamics and in seven severely decompensated chronic congestive heart failure subjects. Each sample was fixed, stained, and photomicrographs of the sections were obtained and the capillary basement membrane thickness determined. The control capillary basement membrane thickness was 3028 plus or minus 187 A (mean plus or minus SEM) compared to the congestive heart failure thickness of 4924 plus or minus 538 A (pless than .01). It is possible that the increased basement membrane thickness in congestive heart failure may result from or actually cause the depressed oxygen consumption by altering diffusion.

Precordial ST segment mapping. A sensitive technique for the evaluation of myocardial injury?

Myocardial ischemic injury was created acutely in pigs by a closed-chest technique utilizing an intracoronary balloon occluder for the interruption of flow in the left anterior descending coronary artery and ST-segment elevation was followed over a two hour period using an 18 lead precordial map. In an experimental group of 10 animals, occlusion was carried out within the left anterior descending coronary artery 8.3 plus or minus 0.5 cm distal to the origin of the main left coronary. Mean ST segment elevation (ST) showed a peak rise of 0.16 mV 10 minutes after occlusion. The balloon was moved proximally 1.6 plus or minus 0.2 cm giving a significant secondary rise of 0.16 mV within 5 minutes, despite indications of a generally small area of additional myocardial involvement, as judged from anatomic distribution of additional vessels occluded as well as a lack of significant change in hemodynamic parameters. In a control group of 5 additional pigs, a single distal occlusion at 6.4 plus or minus 0.9 cm from the origin of the main left coronary was produced by an identical technique. The ST rose to a peak of 0.20 mV at 15 minutes and was followed by a steady decline. Unlike the experimental group, no additonal rise in ST was seen. The technique of precordial mapping thus appears to be a sensitive index of myocardial injury. In addition, it appears from this study that the magnitude of ST elevation is a direct reflection of the extent of myocardial injury.

Quality of life post-myocardial infarction: effects of a transtelephonic coronary intervention system.

The impact of an outpatient, risk-management system, including a transtelephonic electrocardiographic monitor and lidocaine injector, on the quality of life in post-myocardial infarction patients was examined. Patients (n = 238) were assigned randomly to either the system or to standard medical care (control). Quality of life was defined in terms of psychological status, return to work, and social functioning. Relative to control patients, system patients showed a significant decrease in concerns about physical functioning and symptoms, and, over time, reported less depressive affect. At 9-month follow-up, control patients were more than twice as likely to be in the range of clinical depression. Patients' perceptions of their ability to manage a recurrence of cardiac symptoms appeared to be related inversely to depressive affect. Moreover, a larger percentage of system patients (92%) had returned to work by the 9-month follow-up, compared with control patients (76%). There were, however, no significant differences between groups in the degree of impairment in social interaction. Overall, these results indicate that the use of a "system" encouraging patient participation in treatment can significantly improve qualify of life after a myocardial infarction.

Spontaneous multivessel coronary artery dissection: repeated presentation in a healthy postmenopausal woman.

Spontaneous coronary artery dissection is a rare cause of acute myocardial infarction which is infrequently diagnosed antemortem. Most previously reported cases were found in women of whom a significant proportion presented during pregnancy or the postpartum period. We describe the first antemortem case of spontaneous coronary artery dissection, unrelated to pregnancy or the postpartum state, which ultimately resulted in diffuse involvement of both the left and right coronary arteries over a period of 4 months. Pathophysiology and case management of this disorder are discussed.