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Between 1984 and 1993, prevalence and case fatality of hospitalized acute myocardial infarction (AMI) had declined in the population of Halifax County. We aimed to determine whether these trends continued into the 21st century by investigating patient characteristics, treatment methods, and fatality for hospital admissions of residents of Halifax County, aged 25-74, during 1984-1989 (period 1), 1990-1993 (period 2), and 1998-2001 (period 3) and diagnosed as AMI that were extracted from databases for the Halifax County MONICA and ICONS (Improving Cardiovascular Outcomes in Nova Scotia) Studies. Trends in patient characteristics and treatment methods were assessed by chi2 statistics. Their association with 28-day fatality was determined by logistic regression. Event rate declined during 1984-1993 but not into 1998-2001 (p = 0.206). Compared with 1990-1993, fewer AMI patients during 1998-2001 were > or = 55 years (73.3% vs. 69.9%), cigarette smokers (49.8% vs. 42.9%), had a history of myocardial infarction (28.9% vs. 24.9%), and had an admission heart rate >100 (34.8% vs. 17.4%). Additionally, more patients had a history of diabetes (22.5% vs. 28.1%). Case fatality declined progressively over the 3 study time periods (16.6%, 13.1%, and 9.4%, respectively). Changes also occurred in prevalence of Killip class 4 status during admission (20.2%, 10.3%, and 13.3%, respectively), use of thrombolysis (9.0%, 30.9, and 32.6%, respectively), and percutaneous coronary intervention (PCI) (4.3%, 11.2%, and 22.4%, respectively) in the different periods. Significant associations were found between case fatality and patient history of diabetes, history of MI, age, elevated admission heart rate, Killip class 4 impairment, thrombolysis, and PCI. The ICONS registry of hospitalized acute myocardial infarctions was used to compare case fatality during 1998-2001 with that reported by the Halifax County MONICA Project for 1984-1993. Whereas the population rate of myocardial infarctions had declined between 1984-1993 but not subsequently, case fatality declined significantly throughout the study period. The continued decline in case fatality is likely explained by changes in patient profile on presentation and medical therapies, including the increased use of thrombolysis and PCI.

Purpose: Poor documentation in medical records might reduce the quality of care and undermine analyses based on retrospective chart reviews. We assessed the documentation of cardiac risk factors and cardiac history in the records of patients hospitalized with myocardial infarction or heart failure., Methods: We performed a retrospective cohort study involving direct chart audit of all consecutive hospitalizations for myocardial infarction (n = 2,109) or heart failure (n = 3,392) in Nova Scotia, Canada, from October 15, 1997, to October 14, 1998. The main outcome measures were the documentation rates for prespecified clinical items, including cardiac risk factors and history of myocardial infarction or heart failure, which were recognized as indicators of the quality of care for the conditions under study., Results: Information was not documented in a high proportion of cases, ranging from 9% (smoking) to 58% (previous history of heart failure) in charts from patients hospitalized for myocardial infarction, and from 19% (smoking) to 69% (hyperlipidemia) in charts from heart failure hospitalizations. Lack of documentation was more common in women and the elderly., Conclusion: Documentation of important clinical information is poor even in the hospital charts of patients with severe conditions. This quality-of-care issue has implications for health services and outcomes research, including the development of report cards.

Background: A majority of all myocardial infarctions occur in patients who are 65 years of age or older and have average cholesterol levels, but little information is available on whether cholesterol lowering in such patients reduces the rate of recurrent cardiovascular disease., Objective: To determine whether pravastatin reduces the rate of recurrent cardiovascular events in older patients., Design: Subset analysis of a randomized, controlled trial., Setting: 80 hospitals and affiliates in the United States and Canada., Patients: 1283 patients aged 65 to 75 years who had had myocardial infarction and had a plasma total cholesterol level less than 6.2 mmol/L (240 mg/dL) and a low-density lipoprotein cholesterol level of 3.0 to 4.5 mmol/L (115 to 174 mg/dL)., Intervention: Pravastatin, 40 mg/d, or placebo., Measurements: Five-year event rates of major coronary events (coronary death, nonfatal myocardial infarction, angioplasty, or bypass surgery) and stroke., Results: Major coronary events occurred in 28.1% of placebo recipients and 19.7% of pravastatin recipients (difference, 9.0 percentage points [95% CI, 4 to 13 percentage points]; relative risk reduction, 32%; P < 0.001). Coronary death occurred in 10.3% of the placebo group and in 5.8% of the pravastatin group (difference, 4.6 percentage points [CI, 1.9 to 6.5 percentage points]; relative risk reduction, 45%; P = 0.004). Stroke incidence was 7.3% in the placebo group and 4.5% in the pravastatin group (absolute reduction, 2.9 percentage points [CI, 0.3 to 4.5 percentage points]; relative reduction, 40%; P = 0.03). The numbers of older patients needed to treat for 5 years were 11 (CI, 8 to 24) to prevent a major coronary event and 22 (CI, 15 to 53) to prevent a coronary death. For every 1000 older patients treated, 225 cardiovascular hospitalizations would be prevented compared with 121 hospitalizations in 1000 younger patients., Conclusions: In older patients with myocardial infarction and cholesterol levels in the average range, pravastatin is associated with a clinically important reduction in risk for major coronary events and stroke. Given the high cardiovascular event rate in older patients, the potential for absolute benefit in this age group is substantial.

Objectives: This study sought to assess the impact of delaying coronary artery bypass surgery at one Canadian academic tertiary referral center., Background: Universal access to medical services in Canada comes at the expense of waiting lists whose impact has been incompletely assessed., Methods: A prospective, observational study of all residents of Nova Scotia and Prince Edward Island accepted for bypass surgery between 1 April 1992 and 31 October 1992 was undertaken to determine 1) whether triage guidelines were being followed; and 2) the incidence of cardiac death, nonfatal myocardial infarction and worsening symptoms associated with delayed operation. The analysis had 90% power to detect a mortality rate of > or = 3% (alpha 0.05)., Results: Of 423 patients referred, 35% were triaged as urgent, 9.7% as semiurgent A, 39% as semiurgent B and 16.3% as elective, with no age or gender bias identified. Operation occurred at < or = 1 week in 25%, < or = 1 month in 47%, and >6 months in 1.4%. There were no nonfatal myocardial infarctions, but five cardiac deaths occurred (1.2%). Of 275 patients not initially classified as urgent, 12.4% required reclassification to higher priorities because of worsening symptoms; none had perioperative myocardial infarction or died. One in four patients queued longer than target waiting times. Only 4% of patients considered prioritization on the basis of medical need unfair, but 64% experienced at least moderate anxiety., Conclusion: This triage system equitably stratified patients to a queue. Deaths were rare and could not be attributed to the triage process. Patients with worsening clinical status were safely accommodated with earlier waiting times, but concerns remain regarding excessive waiting times and patient anxiety.

We studied the evolution of body-surface potential map (BSPM) patterns in 32 patients following first acute inferior myocardial infarction. Initial BSPMs were obtained at a mean of 79 hours post-infarction; follow-up BSPMs, a mean of eight months post-infarction. Temporal area-of-difference maps, constructed by subtracting initial from follow-up group-mean BSPMs, revealed reciprocal changes over the superior and inferior torso for both Q-zone and ST-segment time-integral distributions. The temporal changes in Q-zone patterns were small but definite: over the inferior torso there was a relative gain in Q-zone values and, over the superior torso, a relative decrease. In contrast, there were marked spatial and quantitative changes of ST-segment distributions during the follow-up period. Over the superior torso, particularly anteriorly, there was a gain in ST-segment values; over the inferior torso, a decrease. With the small temporal changes in Q-zone time-integral distributions, individual Q-zone maps continued to reflect a pattern of inferior myocardial infarction at follow-up. In contrast, the marked temporal changes in ST-segment time-integral distributions resulted in individual map patterns at follow-up that were nearly indistinguishable from normal ST-segment maps. The relatively small changes in depolarization time-integral patterns during the early post-infarction period suggest that the Q-zone patterns of the acute phase of myocardial infarction reflect near-irreversible or completed myocardial damage. The marked normalization of repolarization time-integral patterns during the recovery phase suggests, however, that there are also considerable areas of myocardium-at-risk during the early phase of the infarction process which stabilize with time.

Acute transmural myocardial infarction has been reported to functionally denervate the normal myocardium distal to the infarcted zone by interrupting neurotransmission in axons coursing in the subepicardial region of the myocardial necrosis. To directly investigate the viability of such neurotransmission, the effects of acute transmural myocardial infarction on conduction in the intrinsic cardiac nerves overlying and distal to an experimentally induced acute transmural myocardial infarction were studied. In eight dogs, during control states electrical stimulation of the epicardium adjacent to a coronary artery produced compound action potentials in the more cranially located cardiopulmonary nerves. Thereafter, in four dogs an acute transmural myocardial infarction was produced by injecting rapidly hardening latex into a major diagonal branch of the left anterior descending coronary artery. Epicardial stimulation over the infarct, as well as proximal or distal to it, produced compound action potentials that conducted at normal velocities for at least 12 h postinfarction. The transmural extent of the infarct was verified with tetrazolium blue staining at the end of the experiment. In the other four dogs, compound action potentials were generated in cardiopulmonary nerves as described above and then ventricular fibrillation was produced to assess the effects of global anoxia on the function of axons coursing in cardiac nerves. Following the onset of ventricular fibrillation, compound action potentials were generated in these nerves in C fibers for up to 2 h, in B fibers for up to 4 h, and in A fibers for at least 12 h.(ABSTRACT TRUNCATED AT 250 WORDS)

In order to investigate whether brief, repeated episodes of acute myocardial ischemia impair the function of the intrinsic sympathetic efferent post ganglionic cardiac nerves, 12 cycles of left anterior descending coronary artery occlusions (5 mins) and reperfusions (10 mins) were successfully performed in 10 dogs. Following each brief occlusion percentage systolic shortening in the ventral myocardium was reduced, consistent with myocardial stunning. Stellate ganglion stimulation increased intramyocardial pressures in the ventral and lateral regions of the left ventricle before and after each of the artery occlusions in which stimulations were performed. Isoproterenol and tyramine also augmented intramyocardial pressures in those regions. When the coronary artery was occluded permanently in seven of the dogs tested, stellate ganglion stimulation continued to augment intramyocardial pressure in the ventral region of the left ventricle for up to 35 mins. These results indicate that following repetitive episodes of brief occlusion of a coronary artery that are reported to 'stun' the involved myocardium in a transmural distribution, sympathetic efferent post ganglionic axons can augment inotropism in the affected zone. Furthermore, when a coronary artery is totally occluded thereafter for up to 35 mins these efferent sympathetic post ganglionic nerves continue to function. It is concluded that sympathetic efferent post ganglionic neurons innervating the ventricle can augment cardiac inotropism in a region of stunned myocardium.

To further define the capacity for recovery after acute phase electrical and mechanical injury in patients with Q wave myocardial infarction who were treated with standard measures, 120 lead body surface potential maps and radionuclide angiograms were recorded at day 5 before discharge and month 6 after infarction in 23 patients with a first infarction (12 anterior and 11 inferior by standard 12 lead electrocardiographic criteria). In addition to assessment of spatial changes in electrocardiographic and wall motion patterns, five quantitative variables were evaluated: minimal Q zone integral, sigma Q wave integral, maximal ST integral, left ventricular ejection fraction and left ventricular wall motion abnormality score. From day 5 to month 6 after infarction, the only change in the inferior infarction group was a gain in sigma Q wave (-91 +/- 40 mu V X s X 10(2) to -68 +/- 24 mu V X s X 10(2); p less than 0.05). In contrast, all variables improved over the same time period in the anterior infarction group: Q zone minimum, -34 +/- 20 to -24 +/- 13 mu V X s (p less than 0.05); sigma Q wave, -160 +/- 122 X 10(2) to -120 +/- 90 mu V X s X 10(2) (p less than 0.05); ST maximum, 44 +/- 19 to 18 +/- 9 mu V X s (p less than 0.01); ejection fraction, 54 +/- 7 to 63 +/- 17% (p less than 0.05); and wall motion score, 6 +/- 3 to 3 +/- 3 (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

To define and relate the body surface electrocardiographic and left ventricular wall motion patterns in the acute phase of Q-wave infarction, we recorded 120-lead body surface potential maps and radionuclear angiograms in 29 patients on the fifth day of their first infarction. By standard 12-lead electrocardiographic criteria, 17 patients were designated as anterior infarction and 12 as inferior infarction. Body surface map infarct patterns in the anterior group were characterized primarily by abnormal Q-wave, negative Q-zone and positive ST-segment integral patterns over the anterior torso and little reciprocal change. The maps of the inferior patient group were characterized primarily by depolarization and repolarization infarct patterns over the inferior torso and marked reciprocal changes in all integral patterns over the anterior torso. Both groups displayed infarct patterns over a common area of the right anterior-inferior torso. In the anterior group depolarization minima and repolarization maxima were clustered in a small precordial area; in the inferior group the same extrema were widely scattered over the inferior torso, both anteriorly and posteriorly. Segmental left ventricular wall motion analysis revealed that the 3 most commonly and most severely involved segments were the same in both infarct groups--apical, infero-apical and antero-lateral. Basal septum and antero-basal segmental dysfunction were exclusive to the anterior group; postero-lateral and infero-basal involvement, to the inferior group.(ABSTRACT TRUNCATED AT 250 WORDS)

To gain a correlative perspective of indirect indications of the size of a myocardial infarct, we measured several body-surface electrocardiographic variables and several enzyme and radionuclear angiographic indicators of an infarct's size in 34 patients during the acute phase of first infarction. We found that bivariate correlations ranged widely, from an r value of 0.05 to an r value of 0.92, but were significantly (p less than 0.001) higher when variables from the same technique were correlated (mean r, 0.60 +/- 0.27), as opposed to correlations of variables from different techniques (mean r, 0.27 +/- 0.18). Trivariate comparisons among techniques produced significantly (p less than 0.001) higher r values, but the highest, an r value of 0.76 (total wall motion abnormality score; peak lactic dehydrogenase level; ST-segment integral maximum), indicated that even in this best case, only about 60 percent of the variation of one variable was dependent on or due to the two other variables. These data demonstrate that multiple indirect quantitative indicators of myocardial injury can vary widely in their correlations within the same population of infarcts, and much remains unknown in their relationships during the acute phase. Caution should be exercised, therefore, in their clinical application to predict an infarct's size in individual patients with acute myocardial infarction.

Day 5 body surface map and radionuclide angiographic patterns were compared among 56 patients with first non-Q-wave or Q-wave acute myocardial infarction (AMI). Three radionuclide angiographic patterns were recognized in patients with non-Q infarction: no wall motion abnormalities (n = 8), single-segment wall motion abnormalities (n = 10) and multiple-segment wall motion abnormalities (n = 9). In contrast, only 2 radionuclide angiographic patterns were identified in patients with Q-wave infarction: multiple-segment wall motion abnormalities (n = 25) and single-segment wall motion abnormalities (n = 4). The Q-wave distributions of 14 of 18 patients with non-Q infarction with 0 or 1 wall motion abnormalities were normal; 2 patients had "missed" anterior; 1 patient had inferior; and 1 had posterior AMI patterns. Of 9 patients with non-Q infarction who had multiple-segment wall motion abnormalities, 8 had infarct Q waves on the posterior torso. Q-wave patterns in patients with anterior (n = 17) and inferior (n = 12) Q-wave infarctions were typical and homogeneous for each group. Quantitative analysis of minimum Q-zone integral, sigma Q-wave integrals, ST-integral maximum, wall motion abnormality score and ejection fraction revealed no differences between patients with non-Q-wave and those with inferior Q-wave infarction. In contrast, patients with anterior AMI had significantly more abnormal values of all variables than either of the other groups. Overall, the data support the concept of non-Q-wave AMI as a distinct, if heterogeneous, pathophysiologic entity.(ABSTRACT TRUNCATED AT 250 WORDS)

Perioperative myocardial infarction is a potential consequence of coronary artery bypass surgery. The diagnosis is difficult due to multiple factors including postoperative chest discomfort, serum enzyme elevations and nonspecific electrocardiographic changes. No one test is reliable, but a combination of electrocardiogram, MBCK serum enzyme analysis and technetium pyrophosphate scanning should increase the probability of correct diagnosis. Using this method, the incidence of perioperative myocardial infarction in this study was six out of 100. Left ventricular function in the early postoperative period was adversely affected by perioperative myocardial infarction with a reduction in left ventricular ejection fraction (63 +/- 9% preoperative to 54 +/- 12% postoperative; P less than 0.05), whereas left ventricular ejection fraction was unchanged in the absence of perioperative myocardial infarction. The long term left ventricular function, however, appears to recover, and at two years after surgery there was no difference in rest or exercise left ventricular function between patients who suffered perioperative myocardial infarction versus those who did not. All patients with perioperative myocardial infarction survived to be discharged from hospital, and all returned for follow-up at two years. Their functional and work status was no different from those without perioperative myocardial infarction. This would suggest that, if patients survive a perioperative myocardial infarction, their long term functional status is no different from those patients without perioperative myocardial infarction.