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Biomedical subjects

R S Gibson

Publications and source records attributed to R S Gibson.

At least 91 records · Page 5Linked to original sources

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.

Creatine Kinase↗

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)

Double-Blind Method↗

Comparison of propranolol, diltiazem, and nifedipine in the treatment of ambulatory ischemia in patients with stable angina. Differential effects on ambulatory ischemia, exercise performance, and anginal symptoms. The ASIS Study Group.

Episodes of transient myocardial ischemia during ambulatory activities are common in patients with stable coronary artery disease and who are often asymptomatic. Selection of therapy for episodes of asymptomatic ischemia is limited by a lack of direct comparative studies. To determine the most effective monotherapy for patients with stable angina and a high frequency of asymptomatic ischemic episodes, propranolol-LA (mean daily dose, 293 mg), diltiazem-SR (mean daily dose, 350 mg), nifedipine (mean daily dose, 79 mg) were each compared with placebo, each for 2 weeks, in a randomized, double-blinded, crossover trial. Entry criteria were a positive exercise treadmill test during placebo therapy characterized by 1.0 mm or more ST segment depression and angina pectoris, and six or more episodes of transient ST segment depression of 1.0 mm or more on a 48-hour ambulatory electrocardiogram. One hundred ninety-four patients were screened, 63 were eligible and received randomized therapy, of which 56 patients completed at least two of the four treatment periods and were included in an intent-to-treat analysis. Fifty patients completed all four treatment phases and were included in the protocol-completed analysis. Anti-ischemia efficacy was assessed by 48-hour ambulatory electrocardiographic monitoring, exercise treadmill tests, and anginal diaries. Ninety-four percent of all episodes of ambulatory ischemia were asymptomatic. Compared with placebo, only propranolol was associated with a marked reduction in all manifestations of asymptomatic ischemia during ambulatory electrocardiographic monitoring (2.3 versus 1.0 episodes/24 hr; mean duration of ischemia per 24 hours, 43.6 versus 5.7 minutes; both p less than 0.0001). Diltiazem's reduction of the frequency of episodes compared with placebo (2.3 versus 1.9 episodes/24 hr) was associated with a trend (p = 0.08) in the protocol-completed analysis and with a significant reduction in the intent-to-treat analysis (p = 0.03). Nifedipine had no significant effect on any measured variable of ambulatory ischemia. The dosages of medication used may have been excessive for some patients, and a more beneficial effect may have been evident at a lower dose. In contrast to the marked effects of the active agents on ambulatory asymptomatic ischemia, the effects on exercise performance and angina pectoris were slight. The active agents modestly improved treadmill exercise duration time until 1 mm ST segment depression (3%), and only propranolol and diltiazem had significant effects. Only diltiazem significantly prolonged the total exercise time. Anginal frequency was significantly decreased by both propranolol and diltiazem.(ABSTRACT TRUNCATED AT 400 WORDS)

Angina Pectoris↗

A simplified approach for evaluating multiple test outcomes and multiple disease states in relation to the exercise thallium-201 stress test in suspected coronary artery disease.

This study describes a simplified approach for the interpretation of electrocardiographic and thallium-201 imaging data derived from the same patient during exercise. The 383 patients in this study had also undergone selective coronary arteriography within 3 months of the exercise test. This matrix approach allows for multiple test outcomes (both tests positive, both negative, 1 test positive and 1 negative) and multiple disease states (no coronary artery disease vs 1-vessel vs multivessel coronary artery disease). Because this approach analyzes the results of 2 test outcomes simultaneously rather than serially, it also negates the lack of test independence, if such an effect is present. It is also demonstrated that ST-segment depression on the electrocardiogram and defects on initial thallium-201 images provide conditionally independent information regarding the presence of coronary artery disease in patients without prior myocardial infarction. In contrast, ST-segment depression on the electrocardiogram and redistribution on the delayed thallium-201 images may not provide totally independent information regarding the presence of exercise-induced ischemia in patients with or without myocardial infarction.

Aged↗

Quantitative exercise thallium-201 scintigraphy for predicting angina recurrence after percutaneous transluminal coronary angioplasty.

The aim of this prospective study was to determine the value of quantitative exercise thallium-201 scintigraphy for predicting short-term outcome in patients after percutaneous transluminal coronary angioplasty (PTCA). Quantitative exercise thallium-201 scintigraphy was performed 2.2 +/- 1.2 weeks after successful PTCA in 68 asymptomatic patients, 64 (94%) of whom had class III or IV angina before the procedure. Clinical follow-up was obtained in all patients at a mean of 10 +/- 2 months and all were followed for at least 6 months; 45 patients (66%) remained asymptomatic during follow-up and 23 (34%) developed recurrent class III or IV angina at a mean of 2.6 +/- 1.2 months. Multivariate analysis of 22 clinical, angiographic and exercise test variables revealed that thallium-201 redistribution, any thallium scan abnormality, presence of a distal stenosis and treadmill time were the only significant predictors of recurrent angina after PTCA. Using a stepwise discriminant function model, thallium-201 redistribution was the only significant independent predictor. Despite its prognostic value relative to other variables as a predictor, thallium redistribution at 2 weeks after PTCA was only detected in 9 of the 23 patients (39%) who subsequently developed recurrent angina, although only 2 of the 45 patients (9%) who remained asymptomatic during follow-up demonstrated thallium-201 redistribution at the time of early testing. After repeat angiography was performed in 17 of the 23 patients with recurrent angina, 14 (82%) demonstrated restenosis and 3 (18%) had worse narrowing distal to or remote from the site of dilatation.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗

Effect of the degree of effort on the sensitivity of the exercise thallium-201 stress test in symptomatic coronary artery disease.

The sensitivity of ST-segment depression on the electrocardiogram during exercise is influenced by the level of effort. Whether such is the case with thallium-201 imaging (initial defect or redistribution) has not been established. Accordingly, the prevalence of these parameters was evaluated in 288 patients (age 59 +/- 10 years, 88% men) with coronary artery disease who underwent both exercise thallium-201 imaging and coronary angiography within 3 months of each other: 159 had a prior myocardial infarction, 72 had 1-vessel, and 216 had multivessel disease. The degree of effort was evaluated by 3 criteria: (1) percentage of maximal predicted heart rate (less than or equal to 65, greater than 65 to 85, greater than 85%); (2) workload during exercise (less than or equal to 4, greater than 4 to 8, greater than 8 METs); and (3) duration of exercise (less than or equal to 3, greater than 3 to 6, greater than 6 minutes). The prevalence of defects on initial images was higher than both redistribution on delayed images and ST-segment depression on the electrocardiogram (p less than 0.01). The overall prevalence of initial defects remained the same for all levels of effort and was not influenced by the presence or absence of a prior infarction. However, it decreased in patients with 1-vessel disease who exercised to higher workloads. The prevalence of redistribution on delayed thallium-201 images was higher than that of ST-segment depression on the electrocardiogram (p less than 0.01), except at higher levels of effort where they were similar.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Seasonal variations in hair zinc concentrations in Canadian and African children.

Proximal occipital scalp hair samples were collected during three survey periods from 30 omniverous Canadian boys aged 75.6 +/- 10.4 months (mean +/- SD) and 66 rural Malawian children (37 M; 29 F) aged 62 +/- 10 months (mean +/- SD) consuming predominantly plant-based diets. Hair samples were washed and then analyzed for zinc and copper using instrumental neutron activation analysis. Selected anthropometric measurements were also taken and dietary intakes calculated from weighed dietary records. A marked seasonal variation in hair zinc concentrations occurred in both groups; levels were highest in the season with shortest daylight hours (i.e. December/January in Canada vs July/August in Malawi). A similar trend was not observed for hair copper concentrations. Changes in hair zinc were not associated with changes in growth indices, age, socio-economic group, method of infant feeding, in either group, but were related to intakes of protein (per 1000 kcal) (p = 0.02, r = -0.36), zinc (mg day-1) (p = 0.01, r = -0.39), and dietary fiber (g day-1) (p = 0.04, r = 0.28), in the Malawian children during the second survey period. The seasonal effect on hair zinc concentrations must always be considered when interpreting hair zinc concentrations in children; its etiology remains unclear.

Canada↗

A growth-limiting, mild zinc-deficiency syndrome in some southern Ontario boys with low height percentiles.

A double-blind, pair-matched 12-mo study examined the effects of a zinc supplement (10 mg Zn/d as ZnSO4) on linear growth, taste acuity, attention span, biochemical indices, and energy intakes of 60 boys (aged 5-7 y) with height less than or equal to 15th and midparent height greater than 25th percentiles. Boys with initial hair Zn less than 1.68 mumol/g (n = 16) had a lower mean (+/- SD) weight-for-age Z score (-0.44 +/- 0.59 vs -0.08 +/- 0.84), and a higher median recognition threshold for salt (15 vs 7.5 mmol; p = 0.02) than those with hair Zn greater than 1.68 mumol/g. Only boys with hair Zn less than 1.68 mumol/g responded to the Zn supplement with a higher mean change in height-for-age Z score (p less than 0.05); taste acuity, energy intakes, and attention span were unaffected. A growth-limiting Zn deficiency syndrome exists in boys with low height percentiles, hair Zn levels less than 1.68 mumol/g, and impaired taste acuity.

Body Height↗

Dietary calcium, phytate, and zinc intakes and the calcium, phytate, and zinc molar ratios of the diets of a selected group of East African children.

Dietary zinc, calcium, and phytate intakes of 66 rural Malawian children aged 4-6 y were determined during three seasons on the basis of weighed food records and analyzed food composition data. Height and weight measurements were also recorded and hair samples were collected for zinc analysis. Seasonal daily zinc, calcium, and phytate intakes of females ranged from 6.2 +/- 1.7 to 6.8 +/- 2.1 mg (mean +/- SD), from 335 +/- 170 to 401 +/- 257 mg, and from 1621 +/- 660 to 1729 +/- 592 mg, respectively and, for males, 7.0 +/- 1.7 to 8.0 +/- 2.3 mg, 342 +/- 164 to 473 +/- 310 mg, and 1857 +/- 530 to 2161 +/- 684 mg, respectively. Cereals provided greater than 42% of dietary zinc. Seasonal mean molar ratios of phytate to Zn and Ca x phytate to Zn [per 1000 kcal (4.2 MJ)] and the median Ca to phytate molar ratio ranged from 24 to 27, 151 to 188 mmol/1000 kcal (4.2 MJ), and 3.1 to 3.4, respectively. Over 78% of the children consumed diets with phytate-to-Zn and Ca x phytate.Zn-1 . 1000 kcal-1 molar ratios above values suggested to jeopardize zinc status. Correlations between hair zinc, phytate-to-Zn, and Ca x phytate.Zn-1 . 1000 kcal-1 molar ratios suggest that high phytic acid intakes may compromise zinc status in these children.

Body Height↗

Prevention of reinfarction subsequent to non-Q-wave infarction.

A multicenter, double-blind, randomized study was performed to evaluate the cardioprotective effects of diltiazem administered to patients with MB creatine kinase-confirmed acute non-Q-wave myocardial infarction. Nine centers enrolled a total of 576 patients, with 287 receiving diltiazem and 289 receiving placebo (90 mg every 6 h). Treatment was started 24-72 h after onset of clinical infarction and continued for up to 14 days. The primary endpoint was recurrent myocardial infarction, which was defined as an abnormal reelevation in plasma MB creatine kinase during the 14-day study period. MB creatine kinase samples were obtained every 12 h after randomization and were assayed by a central core laboratory using the glass bead adsorption method. Recurrent myocardial infarction was documented in 27 patients in the placebo group (9.3%) versus 15 patients in the diltiazem group (5.2%)--reflecting a reduction of 51.2% in the cumulative life-table reinfarction rate (p = 0.0297). The significance of this difference for treatment effect remained at a comparable alpha-level after individual adjustments (Cox model) for age, gender, previous infarction, obesity, site of qualifying infarction, Killip Class at entry, and concurrent use of beta-blocking agents. Diltiazem also reduced the incidence of refractory postinfarction angina necessitating study withdrawal, and angina associated with transient ST-T changes by 49.7% (p = 0.0345) and by 28% (p = 0.0057), respectively. Atrioventricular block, bradycardia, hypotension, and sinus pauses were more common in patients receiving diltiazem, but the drug was well tolerated overall despite the fact that 61% of diltiazem patients were also taking beta-blockers. These results indicate that high-dose diltiazem is well tolerated, safe, and effective in the prevention of early reinfarction and severe angina after non-Q-wave infarction.

Adult↗

Favourable long term prognosis in patients with non-Q wave acute myocardial infarction not associated with specific electrocardiographic changes. Diltiazem Reinfarction Study Research Group.

Electrocardiograms obtained serially from 544 patients with non-Q wave infarction in the Diltiazem Reinfarction Study were analysed to compare the short term (less than or equal to 14 days) and long term (one year) follow up of 105 patients (19%) whose admission electrocardiogram showed no localisable repolarisation abnormalities (group 1) with the outcome in 439 patients (81%) who had ST-T wave abnormalities (group 2) localised to two or more contiguous leads within an anterior, inferior, or lateral lead group. There were no major between group differences in baseline clinical variables, concomitant medications, or treatment allocation (diltiazem v placebo). Group 2 patients, in the first year, had a higher incidence of early recurrent ischaemia (angina greater than or equal to 24 hours after myocardial infarction associated with ischaemic repolarisation changes), reinfarction, and readmission for chest pain than group 1 patients, despite comparable creatine kinase and creatine kinase MB activities in both groups. About 20% of patients with acute non-Q wave myocardial infarction did not have definable ST-T wave abnormalities. These patients had a similar clinical and enzymatic profile as patients with non-Q wave infarction with definable ST-T wave abnormalities and they were more likely to have a favourable short term and long term outcome.

Creatine Kinase↗

Hair chromium as an index of chromium exposure of tannery workers.

The use of hair chromium (Cr) concentrations as an index of Cr exposure of tannery workers was investigated. As has been shown earlier, Cr from Cr III compounds used in the leather tanning industry is absorbed because concentrations of Cr in serum and urine of tannery workers are significantly increased compared with corresponding concentrations for unexposed controls. Hair samples were collected from 71 male tannery workers from four southern Ontario tanneries and from 53 male controls not exposed to Cr in the workplace. Subjects were matched for age, race, and socioeconomic status. Hair samples were washed, ashed in a low temperature asher, and analysed by flameless atomic absorption. The median hair Cr concentrations for the tannery workers (551 ng/g) was significantly higher (p = 0.0001) than for the controls (123 ng/g). For the tannery workers, hair Cr concentrations were positively and significantly correlated with serum Cr (r = 0.52, p less than 0.01) and with the preshift and postshift urinary Cr/creatinine ratios (r = 0.43, p less than 0.01; r = 0.64, p less than 0.01, respectively). These data indicate that trivalent Cr absorbed from leather tanning compounds results in raised concentrations of Cr in hair and that hair Cr concentrations may be used as an index of industrial Cr exposure.

Adult↗

Non-Q-wave myocardial infarction: pathophysiology, prognosis, and therapeutic strategy.

Non-Q-wave infarction, formerly referred to as nontransmural infarction, is usually associated with less myocardial necrosis and a lower in-hospital mortality than Q-wave or transmural infarction. Despite the initially favorable prognosis, however, long-term survival of patients after non-Q-wave infarction is similar to or even shorter than that after Q-wave infarction. It is now well documented that patients with non-Q-wave infarction are more prone to reinfarction, which usually occurs in the same area as the original injury. Since extensive damage from recurrent myocardial necrosis has a considerable deleterious effect on long-term survival, patients with non-Q-wave infarction would be expected to benefit from prophylactic treatment that prevents reinfarction. Indeed, this subset of patients appears to provide a unique opportunity to modify favorably the natural history of ischemic heart disease.

Adrenergic beta-Antagonists↗

ST segment shifts are poor predictors of subsequent Q wave evolution in acute myocardial infarction. A natural history study of early non-Q wave infarction.

Acute ST segment elevation is regarded generally as the sine qua non of evolving Q wave myocardial infarction (MI) because such electrocardiographic (ECG) injury is believed to be a marker of transmural ischemia and a forerunner of transmural necrosis. Alternatively, ST segment depression with or without T wave inversion is viewed as the dominant ECG feature of non-Q wave MI. However, this hypothesis has not been assessed prospectively in an acute MI population. We analyzed 2,304 serial ECGs at study entry (admission), day 2, day 3, and predischarge (mean, 10.2 +/- 2 days) from 576 patients with creatine kinase MB confirmed acute non-Q wave MI to determine what percentage of patients with early ST segment elevation culminated in subsequent Q wave development. Of this group, 187 patients (32%) exhibited 1 mm or greater ST segment elevation in two or more contiguous entry ECG leads. Of those patients whose non-Q wave MI could be localized on the basis of diagnostic admission ST segment shifts, the prevalence of early ST segment elevation was 43% (187 of 439). The sum total mean (+/- SD) peak ST segment elevation by lead group (anterior, inferior, lateral) was 4.0 +/- 2.4, 4.5 +/- 2.4, and 2.5 +/- 0.6 mm, respectively. Despite this, only 20% of patients with ST segment elevation (37 of 187) developed Q waves. Of 252 patients who exhibited early ST segment depression or T wave inversion or both, 39 (15%) evolved subsequent Q waves. Thus, while the prevalence of early ST segment elevation in acute evolving non-Q wave MI was higher than previously reported, 80% of patients with and 85% of patients without ST segment elevation and absent Q waves on the admission ECG did not develop subsequent Q waves during a 2-week period of observation (p = NS). In addition, when patients with ST segment elevation were compared with patients with ST segment depression or T wave inversions or both, there were no between-group differences in log peak creatine kinase (404 vs. 383 IU), reinfarction (6% vs. 8%), postinfarction angina (50% vs. 42%), or early recurrent ischemia (49% vs. 45%), defined as postinfarction angina with transient ECG changes. Thus, in patients who present with initial acute non-Q wave MI, ST segment shifts on admission are unreliable predictors of subsequent Q wave evolution and do not discriminate significant differences in postinfarction outcome. In particular, ST segment elevation during the early hours of evolving infarction is not an invariable harbinger of subsequent Q wave development.

Creatine Kinase↗

Risk stratification of patients with non-Q wave myocardial infarction. The critical role of ST segment depression. The Diltiazem Reinfarction Study Research Group.

One-year follow-up data on 515 patients who survived hospitalization with MB-creatine kinase-confirmed, acute non-Q wave myocardial infarction were analyzed for factors related to mortality (n = 57) and late reinfarction (n = 64). Twelve of 24 analyzed variables were significantly associated with mortality. Those factors, which were independently predictive of mortality by Cox regression analysis, were persistent ST depression (p = 0.0009), a history of congestive heart failure (CHF) (p = 0.0069), older age (p = 0.0128), and ST elevation at hospital discharge (p = 0.0173). In-hospital reinfarction achieved borderline significance (p = 0.0512). Mortality during the follow-up period was 5.5% in patients with no ST depression, 10.1% in those with ST depression at baseline or discharge, and 22.2% in patients with ST depression at baseline and discharge (i.e., "persistent" ST depression). The age-adjusted risk of mortality for patients with persistent ST depression, discharge-ST elevation, and CHF was 13.99 times as high as was the risk for patients with no ST depression, no discharge-ST elevation, and no CHF. Of the 483 patients with complete electrocardiographic data at both baseline and discharge, 203 (42%) could be stratified into a high risk population with a risk ratio for 1-year mortality more than sevenfold that of patients with no risk factors. Although persistent ST depression was significantly associated with several measures of structural left ventricular damage, the independent significance of ST depression persisted even after adjusting for these factors. The independent predictors of late reinfarction (persistent ST depression, p = 0.0058; Killip class II or III, p = 0.0106; and left ventricular hypertrophy, p = 0.0470) permitted a similar risk stratification. We conclude that 1) easily identified clinical and electrocardiographic factors permit stratification of patients with non-Q wave infarction into high-risk subsets who may benefit from aggressive therapy; 2) ST depression is a highly significant and independent predictor of poor prognosis; and 3) the powerful predictive value of persistent ST depression suggests that non-Q wave myocardial infarction patients with this depression should be viewed as potentially high-risk patients who may be candidates for additional noninvasive testing or early coronary angiography.

Diltiazem↗

Current status of calcium channel-blocking drugs after Q wave and non-Q wave myocardial infarction.

The calcium channel blockers are useful in treating many cardiovascular disorders. Due to their anti-ischemic and spasmolytic properties, the cardioprotective effects of these agents have been studied in the setting of acute myocardial infarction. This paper will review this application with respect to limitation of infarct size, reduction of mortality, and incident morbidity rates. Of the agents currently available for clinical use, nifedipine has been studied most extensively. This agent shows no beneficial effects and its use can, in fact, be harmful in this setting. Of the few trials that have been conducted with verapamil, none have shown a preventive effect on death, reinfarction, or postinfarction angina. Both verapamil and diltiazem might limit infarct size although further confirmation is required. At the present time, diltiazem is the only agent shown to have short- and long-term benefits on clinical outcome in patients with acute myocardial infarction. The success of prophylactic diltiazem is, however, critically dependent on proper patient selection. In particular, those patients with non-Q wave infarction, normal left ventricular function, or both can be expected to derive the greatest benefit in terms of reduced mortality and incident morbidity.

Adrenergic beta-Antagonists↗

Management of acute non-Q-wave myocardial infarction: role of prophylactic pharmacotherapy and indications for predischarge coronary arteriography.

Non-Q-wave myocardial infarction (MI) differs from Q-wave MI in three important respects: (1) smaller infarct size possibly due to early reperfusion as a result of spontaneous thrombolysis, relief of spasm, or both; (2) more frequent patency of the infarct-related artery; and (3) a larger residual mass of viable but jeopardized myocardium within the perfusion zone of the infarct-related vessel. Left ventricular function, unless impaired by previous MI, is generally better. The prognosis is worse after the acute phase, when residual ischemia is present, and reinfarction rates during hospitalization and in the subsequent year of follow-up are higher. Obviously, since myocardial ischemia is potentially reversible, its presence should be energetically sought in all patients with recognized non-Q-wave MI. Based on our current understanding and available data, the following guidelines for the management of non-Q-wave MI patients can be recommended: (1) antiplatelet therapy along with diltiazem should be administered to patients as soon as the diagnosis is established, unless contraindications exist; (2) patients who develop early recurrent ischemia on therapy, that is, angina with associated ST-T-wave changes, should undergo prompt cardiac catheterization and myocardial revascularization; (3) patients with entirely uncomplicated hospital courses who are asymptomatic should undergo exercise stress testing, preferably in conjunction with thallium-201 imaging, before hospital discharge. Only those with evidence of significant residual ischemia need cardiac catheterization and myocardial revascularization.

Adrenergic beta-Antagonists↗