Definite Acute Myocardial Infarction Research Articles

Diagnostic Value of High-Sensitivity Cardiac Troponin-I in Patients After Out-of-Hospital Cardiac Arrest

Knowing the etiology of cardiac arrest (CA) is important for treatment decisions. Results of previous studies on the diagnostic role of cardiac troponin in patients resuscitated from CA are controversial, few studies were done during the era of high-sensitivity cardiac troponin-I (hs-cTnI), and kinetics of hs-cTnI was not thoroughly investigated. We aimed to explore the diagnostic value of hs-cTnI in patients resuscitated from out-of-hospital CA (OHCA). This retrospective study included 201 consecutive patients after OHCA admitted to the intensive cardiac care unit at Rambam Health Care Campus from 2016 to 2021. Patients were divided into 2 groups according to etiology of CA: group 1-patients with definite acute myocardial infarction (AMI), group 2-patients in whom AMI was excluded. Values of hs-cTnI on admission, peak hs-cTnI, and hs-cTnI upslope were compared between patients with AMI and non-AMI. Peak hs-cTnI and hs-cTnI upslope differed significantly between patients with non-AMI versus AMI CA (median 1,424 vs 32,558ng/L, p<0.0001 and median 109 vs 2,322ng/L/h, p<0.0001, respectively). Moreover, peak hs-cTnI and hs-cTnI upslope were found to have good discrimination performance between patients with non-AMI and AMI, with area under the curve receiver operating characteristics (ROC) curves of 0.83 and 0.80, respectively. In conclusion, in patients resuscitated from OHCA values of peak hs-cTnI and hs-cTnI upslope could be helpful in the diagnosis of etiology of CA as adjunct to other diagnostic methods.

Circadian and seasonal variation in onset of acute myocardial infarction.

The aim was to investigate the circadian and seasonal variation of acute myocardial infarction (AMI). Clinical data of 3867 AMI patients hospitalized from November 2010 to October 2019 in the Border Yanbian Minority Autonomous Prefecture, China were collected, and 3158 patients with definite AMI onset times were analyzed. The clinical data analyzed included the time of onset, nationality, age, laboratory data. We divided the patients into 4 groups based on the timepoint of their AMI onsets: 00:00-05:59, 06:00-11:59, 12:00-17:59, and 18:00-23:59. We also divided the patients based on nationality: Chinese Korean and Han groups. We observed that there is a circadian rhythm in the incidence of AMI, and the peak of AMI is in the morning (7:00-9:00). Unexpectedly, the incidence of AMI was significantly lower in the cold winter than that of other 3 warm seasons (P < 0.01) and the peak of AMI presented at the months of the large contrast between day and night temperature difference (over 20°C) like May of Spring and October of Fall. Finally, there was no difference in circadian rhythm between Chinese Korean and Han, although these groups differed in age, body mass index, and the inflammatory cell level. These findings have shown a different seasonal and circadian variation in onset of AMI. Further studies are required to determine the pathophysiological mechanism(s) underlying these differences and to guide prevention of AMI for reducing its mortality and disability.

Science, Medicine, and the Anesthesiologist

Science, Medicine, and the Anesthesiologist

Lack of association between cystatin C and different coronary atherosclerotic manifestations

Cystatin C (CysC) is known to be related to cardiovascular disease (CVD), including the presence and severity of coronary artery disease (CAD) and future clinical events. In this study, the association between CysC levels and (1) coronary artery calcification (CAC) in asymptomatic individuals from the general population as well as (2) different subgroups of patients with suspected or definite acute myocardial infarction (MI) was investigated. CysC levels were measured in serum from asymptomatic individuals as part of a screening study for CAC using non-contrast cardiac CT scan (N = 1039) as well as in subgroups of hospitalized patients with a suspected MI (N = 769). CysC was not associated with CAC in asymptomatic individuals after adjusting for relevant risk factors. No difference in CysC levels was observed between patients with type 1 MI (1.07 mg/L) and patients with normal troponin (with or without prior CAD: 1.14 and 1.01 mg/L, respectively). However, patients with type 2 MI and patient subgroups with elevated troponin but without MI had significantly higher CysC levels (1.24, 1.23 and 1.31 mg/L), even after adjusting for other risk factors. CysC was not associated with CAC in middle-aged asymptomatic individuals from the general population. Furthermore, CysC levels were found to be significantly lower in patients with type 1 MI compared to patients with type 2 MI and patients with elevated troponins but without MI. Thus, in two independent and clinically different populations, no association between CysC and coronary atherosclerotic manifestations could be demonstrated.

Diagnostic and Prognostic Utility of Circulating Cytochrome c in Acute Myocardial Infarction.

In contrast to cardiomyocyte necrosis, which can be quantified by cardiac troponin, functional cardiomyocyte impairment, including mitochondrial dysfunction, has escaped clinical recognition in acute myocardial infarction (AMI) patients. To investigate the diagnostic accuracy for AMI and prognostic prediction of in-hospital mortality of cytochrome c. We prospectively assessed cytochrome c serum levels at hospital presentation in 2 cohorts: a diagnostic cohort of patients presenting with suspected AMI and a prognostic cohort of definite AMI patients. Diagnostic accuracy for AMI was the primary diagnostic end point, and prognostic prediction of in-hospital mortality was the primary prognostic end point. Serum cytochrome c had no diagnostic utility for AMI (area under the receiver-operating characteristics curve 0.51; 95% confidence intervals 0.44-0.58; P=0.76). Among 753 AMI patients in the prognostic cohort, cytochrome c was detectable in 280 (37%) patients. These patients had higher in-hospital mortality than patients with nondetectable cytochrome c (6% versus 1%; P<0.001). This result was mainly driven by the high mortality rate observed in ST-segment-elevation AMI patients with detectable cytochrome c, as compared with those with nondetectable cytochrome c (11% versus 1%; P<0.001). At multivariable analysis, cytochrome c remained a significant independent predictor of in-hospital mortality (odds ratio 3.0; 95% confidence interval 1.9-5.7; P<0.001), even after adjustment for major clinical confounders (odds ratio 4.01; 95% confidence interval 1.20-13.38; P=0.02). Cytochrome c serum concentrations do not have diagnostic but substantial prognostic utility in AMI.

Abstract 56: Prognosis of Patients with Acute Myocardial Infarction by Hospital Discharge Diagnosis

Background: Research on acute myocardial infarction (AMI) in medical claims largely focuses on hospitalizations where AMI is the primary discharge diagnosis (dx). Limited data are available on AMIs occurring as a secondary dx during hospitalization. Hypothesis: We hypothesized that mortality following AMI is higher when the primary dx is not AMI. Methods: We examined REasons for Geographic And Racial Differences in Stroke (REGARDS) study participants with definite or probable AMIs adjudicated using published guidelines. Participants were categorized by hospital discharge dx from the discharge summary: primary dx, secondary dx, or no dx of AMI. All-cause and cardiovascular mortality after AMI, detected though active follow-up and the National Death Index, were compared using Kaplan-Meier curves with log-rank tests and Cox proportional hazard models adjusted for sociodemographics, medical history, and characteristics of the AMI (clinical evidence of ischemia, peak troponin, and heart failure during hospitalization). Results: Of 877 participants with AMI, 37% had AMI as primary dx, 12% had AMI as a secondary dx, and 51% had no dx of AMI. All-cause mortality (n = 284) was higher among participants with AMI as a secondary dx or without a dx of AMI than among participants with AMI as primary dx, but cardiovascular mortality (n = 150) was similar across groups ( Figure ). Compared to participants with AMI as primary dx, adjusted hazard ratios for all-cause mortality were 1.03 (95% CI 0.68-1.57) and 1.17 (95% CI 0.84-1.62) and for cardiovascular mortality were 0.79 (95% CI 0.46-1.37) and 0.91 (95% CI 0.60-1.38) for participants with AMI as a secondary dx and without a dx of AMI, respectively. Conclusions: Studies of AMI based on primary discharge dx likely under count the number of AMIs and exclude a population with similar prognosis in terms of all-cause and CVD mortality, once clinical differences considered. Further study into the characteristics, in-hospital and post-discharge management of these patients may be warranted.

Implications of changing definitions of myocardial infarction on number of events and all-cause mortality: the WHO 1979, ESC/ACC 2000, AHA 2003, and Universal 2007 definitions revisited

To analyse the impact of four different definitions of acute myocardial infarction (AMI) on number of events and all-cause mortality after AMI. We retrospectively examined number of AMI events and mortality according to four different definitions of AMI, among 1494 patients admitted to Haukeland University Hospital in Norway from March 2002 to February 2003. Eligible for analysis were 815 patients with a discharge diagnosis of an AMI, and 679 patients without any AMI discharge diagnosis but with elevated cardiac troponin I level during admission. Applying the WHO 1979 definition resulted in 566 definite AMIs among the 1494 patients and was used as reference. According to the other definitions, there were 455 (-20%) definite AMIs by the original troponin 'rise and fall' version of the ESC/ACC 2000 definition, 729 (+29%) by the troponin 'rise or fall' interpretation of the ESC/ACC 2000 definition, 761 (+34%) by the AHA 2003 definition, and 743 (+31%) by the Universal 2007 definition (all p < 0.001). The 28-day, 1-year, 5-year, and 8-year mortality for definite AMI applying the WHO 1979 definition was 12, 19, 32, and 40%, whereas applying the Universal 2007 definition resulted in a mortality of 14, 21, 35, and 43%, respectively. The change of definitions of AMI during the last decades has had a significant impact on the number of AMI events and a moderate impact on the AMI mortality among hospitalized patients.

Comparison of C‐reactive Protein and Albumin Excretion as Prognostic Markers for 10‐Year Mortality After Myocardial Infarction

C-reactive protein (CRP) is an established prognostic marker in the setting of acute coronary syndromes. Recently, albumin excretion rate also has been found to be associated with adverse outcomes in this clinical setting. Our aim was to compare the prognostic power of CRP and albumin excretion rate for long-term mortality following acute myocardial infarction (AMI). To determine whether albumin excretion rate is a better predictor of long-term outcome than CRP in post-AMI patients. We prospectively studied 220 unselected patients with definite AMI (median [interquartile] age 67 [60-74] y, female 26%, heart failure 39%). CRP and albumin-to-creatinine ratio (ACR) were measured on day 1, day 3, and day 7 after admission in 24-hour urine samples. Follow-up duration was 10 years for all patients. At survival analysis, both CRP and ACR were associated with increased risk of 10-year all-cause mortality, also after adjusting for age, hypertension, diabetes mellitus, prehospital time delay, creatine kinase-MB isoenzyme peak, heart failure, and creatinine clearance. CRP and ACR were associated with nonsudden cardiovascular (non-SCV) mortality but not with sudden death (SD) or noncardiovascular (non-CV) death. CRP was not associated with long-term mortality, while ACR was independently associated with outcome both in short- and long-term analyses. At C-statistic analysis, CRP did not improve the baseline prediction model for all-cause mortality, while it did for short-term non-SCV mortality. ACR improved all-cause and non-SCV mortality prediction, both in the short and long term. ACR was a better predictor of long-term mortality after AMI than CRP.

Lack of association between left bundle-branch block and acute myocardial infarction in symptomatic ED patients

Objective Guidelines recommend treating patients with a new or presumed new left bundle-branch block (LBBB) similar to those with an acute ST-segment elevation myocardial infarction. It is often unclear which emergency department (ED) patients with potentially ischemic symptoms actually have an acute myocardial infarction (AMI), even in the setting of LBBB. Our null hypothesis was that in ED patients with potential AMI, the presence of a new or presumed new LBBB would not predict an increased likelihood of AMI. Methods This was an observational cohort study. Patients older than 30 years who presented with chest pain or other ischemic equivalent and had an electrocardiogram (ECG) to evaluate potential acute coronary syndrome (ACS) were enrolled. Data collected include demographics, history, ECG, and cardiac markers. Electrocardiograms were classified according to the standardized guidelines, including LBBB not known to be old (new or presumed new LBBB), LBBB known to be old, or no LBBB. The hospital course was followed, and 30-day follow-up was performed on all patients. Our main outcome was AMI. Results There were 7937 visits (mean age, 54.3 ± 15 years, 57% female, 68% black): 55 had new or presumed new LBBB, 136 had old LBBB, and 7746 had no LBBB. The rate of AMI was not significantly different between the 3 groups (7.3% vs 5.2% vs 6.1%; P = .75). Revascularization (7.8% vs old 5.2% vs 4.3%; P = .04) and coronary artery disease were more common in patients with new or presumed new LBBB (19.2% vs 11.9% vs 10.1%; P = .0004). Conclusions Despite guideline recommendations that patients with potential ACS and new or presumed new LBBB should be treated similar to STEMI, ED patients with a new or presumed new LBBB are not at increased risk of AMI. In fact, the presence of LBBB, whether new or old, did not predict AMI. Caution should be used in applying recommendations derived from patients with definite AMI to ED patients with potential ACS that may or may not be sustaining an AMI.

Atrial fibrillation during acute myocardial infarction: association with all-cause mortality and sudden death after 7-year of follow-up

Atrial fibrillation/flutter (AF/FL) is a common complication of acute myocardial infarction (AMI). Indeed, the determinants of AF/FL in AMI-patients and the association of AF/FL with mortality are not well-known. The purpose of the present study was to investigate the relationship between presence of AF/FL and mortality in patients with AMI and to report on predictors of AF/FL. We studied 505 patients enrolled in three intensive care units with definite AMI and followed up for 7 years. No patient was lost to follow-up. Patients with AF/FL during the 1st week of hospitalisation were compared with those with steady sinus rhythm. End-points were all-cause mortality and modes of death. At multivariable logistic regression analysis, elderly, body mass index, congestive heart failure (CHF), history of hypertension and plasma cholesterol (in a negative fashion) were independently associated with the presence of AF/FL. At survival analysis, after full adjustment, AF/FL was not associated with in-hospital mortality. After 7 years of follow-up, AF/FL was found to be associated with all-cause mortality [adjusted odds ratio (OR) = 1.6; 95% confidence interval (CI) = 1.2-2.3], together with age, diabetes mellitus, creatine kinase-MB isoenzyme (CK-MB) peak, CHF, estimated glomerular filtration rate and thrombolysis. At adjusted logistic polynomial regression analysis, AF/FL was found to be associated with an excess of mortality for reasons of sudden death (SD) (adjusted OR = 2.7; 95% CI = 1.2-6.4). No interaction was observed between AF/FL and medications on in-hospital mortality. For 7-year mortality, angiotensin-converting enzyme (ACE)-inhibitors and digitalis showed an independent negative (protective) interaction chiefly on SD (adjusted OR = 0.06; 95% CI = 0.01-0.74, and RR = 0.10; 95% CI = 0.02-0.58, respectively). Patients with AMI and AF/FL portend a poor prognosis in the long-term chiefly because of an excess of SD. Treatment with ACE-inhibitors and digitalis may have long-term beneficial effects on SD.

Long term survival after evidence based treatment of acute myocardial infarction and revascularisation: follow-up of population based Perth MONICA cohort, 1984-2005

Objective To examine trends in long term survival in patients alive 28 days after myocardial infarction and the impact of evidence based medical treatments and coronary revascularisation during or near...

Temporal trends in the frequency and longer‐term outcome of heart failure complicating myocardial infarction

To investigate trends in incidence and long-term outcome of heart failure (HF) developing within 28 days of first-ever acute myocardial infarction (AMI). We identified all residents of Perth, Western Australia aged 25-64 years, with no history of HF, who experienced a non-fatal, first-ever AMI between 1984 and 1993, and followed them for ten years. All patients (N=4006) met the criteria for 'definite AMI' in WHO MONItoring trends and determinants of CArdiovascular disease (MONICA) Project and 897 (22.4%) had early-onset HF complicating the index event. After adjustment for age, current smoking, history of diabetes and hypertension, Q-wave and anterior wall AMI, the odds of developing HF declined by 9% (odds ratio for period 1989-1993 relative to 1984-1988=0.91, 95% confidence interval (95%CI): 0.78 to 1.06). Over 10 years of follow-up, patients with early-onset HF had a cumulative average number of re-admissions of 28 per 100 as compared with 9 per 100 in patients without HF. After adjustment for age, history of diabetes and hypertension, the hazard of death in patients with early-onset HF declined by 26% (HR for the period 1989-1993 relative to 1984-1988=0.74, 95%CI: 0.57 to 0.96). Our data suggest a decline in the incidence of, and show encouraging evidence of improvement in survival after, early-onset HF complicating AMI.

Elevated Troponin Levels Are Associated with Sympathoadrenal Activation in Acute Ischaemic Stroke

Background: It has been hypothesised that elevated serum troponin levels in acute stroke are due to myocardial damage caused by sympathoadrenal activation, which, in turn, may be due particularly to insular damage. We aimed to determine the factors associated with troponin elevation in ischaemic stroke and the prognostic value of this finding. Methods: We studied 222 consecutive acute ischaemic stroke admissions. Serum troponin I and catecholamines were measured. Ischaemic damage on brain computed tomography (CT) scan was graded using the Alberta Stroke Program Early CT Score (ASPECTS). Electrocardiograms were classified using the Minnesota Code and the European Society of Cardiology/American College of Cardiology criteria for acute myocardial infarction. The Rankin scale was recorded at 30 days. Results: Forty-five patients (20%) had troponin I >0.2 µg/l. These troponin-positive patients had higher epinephrine levels (median 0.27 vs. 0.17 nmol/l; p = 0.0002) and were more likely to have electrocardiograms coded as definite or possible acute myocardial infarction (odds ratio 3.35; 95% CI 1.26–8.93), compared with those with troponin ≤0.2 µg/l, in univariate analysis. There were no significant associations between troponin I score and ASPECTS or insular damage on brain CT. In logistic regression analyses, elevated troponin was significantly associated with age, elevated serum creatinine and epinephrine; however, increased troponin was not an independent predictor of death or dependency (Rankin >2) at 30 days. Conclusions: Raised troponin I is associated with elevation of circulating epinephrine in acute ischaemic stroke. Activation of the sympathoadrenal system may be an important contributor to myocardial damage in these patients. Increased troponin is not associated with insular damage and does not independently predict poor outcome.

C‐reactive protein, heart rate variability and prognosis in community subjects with no apparent heart disease

Increased C-reactive protein (CRP) and reduced heart rate variability (HRV) both indicate poor prognosis. An inverse association between HRV and CRP has been reported, suggesting an interaction between inflammatory and autonomic systems. However, the prognostic impact of this interaction has not been studied. We thus investigated the prognostic impact of CRP, HRV and their combinations. Population-based study. A total of 638 middle-aged and elderly subjects with no apparent heart disease from community. All were studied by clinical and laboratory examinations, and 24-h Holter monitoring. Four time domain measures of HRV were studied. All were prospectively followed for up to 5 years. Mean age was 64 years (55-75). During the follow-up, 46 total deaths and 11 cases of definite acute myocardial infarction were observed. Both CRP and three of four HRV measures were significantly associated with increased rate of death or myocardial infarction. In a Cox model with CRP >or=2.5 microg mL(-1), standard deviation for the mean value of the time between normal complexes <or=100 ms, and their combination, hazard ratio and 95% CI for subjects with both abnormalities was 3.20 (1.55-6.56), P = 0.0016, and for subjects with either abnormality 1.63(0.83-3.20), P = 0.15, after adjustment for conventional risk factors. The combination of CRP and other measures of HRV gave similar results. This indicates an interaction between CRP and HRV with a synergistic effect. The combination of CRP and HRV or heart rate (HR) predicts death and myocardial infarction with synergism, indicating interaction between inflammatory and autonomic systems with a prognostic significance.

Prevalence of aspirin resistance in patients with an evolving acute myocardial infarction

Objective To study the prevalence and importance of aspirin resistance in patients with an evolving acute myocardial infarction (AMI) by use of the Platelet Function Analyzer-100. Introduction Previous studies have demonstrated the existence of aspirin resistance, but the clinical relevance of the phenomenon remains to be clarified. If aspirin resistant patients comprise a high-risk subgroup, it might be expected that the prevalence of aspirin resistance in patients with AMI would be higher than in patients without AMI. We hypothesized that the prevalence of aspirin resistance in patients with AMI was twice the prevalence in patients without AMI. Methods We included 298 consecutive patients with known cardiovascular disease who were admitted to hospital with symptoms suggestive of an AMI. All had been taking aspirin 150 mg/day for at least 7 days prior to hospital admission. Platelet function was measured immediately at admission, and aspirin resistance was defined as a collagen/epinephrine Closure Time (CT CEPI) < 165 s. Results We found that 70 (23.5%) patients were aspirin resistant, and 70 (23.5%) patients ended up with the diagnosis of an AMI. The prevalence of aspirin resistance was significantly higher in patients with AMI as compared to patients without (36% versus 20%, OR 2.26, CI 95% 1.19–4.22, p = 0.0058). The CT CEPI measured at admission was an independent factor associated with an AMI. Conclusions Aspirin resistance is present in almost one fourth of patients admitted to hospital with symptoms suggestive of an AMI, and aspirin resistance is significantly associated with the diagnosis of a definite AMI.

Congestive heart failure with preserved left ventricular systolic function after acute myocardial infarction: clinical and prognostic implications.

To characterise the prevalence, in-hospital complications, management, and long-term outcome of patients with congestive heart failure but preserved left ventricular systolic function after acute myocardial infarction. 3166 consecutive patients screened for entry in the Bucindolol Evaluation in Acute Myocardial Infarction Trial with definite acute myocardial infarction and echocardiographic assessment of left ventricular systolic function were included between 1998 and 1999 in this prospective observational study. Main outcome measures were occurrences of in-hospital complications and all cause mortality. Congestive heart failure was seen during hospitalisation in 1464 patients (46%), 717 patients had preserved left ventricular systolic function (wall motion index > or =1.3 corresponding to ejection fraction > or =0.40), and 732 patients had systolic dysfunction (wall motion index <1.3). One year mortality in patients with no heart failure, heart failure with preserved systolic function, and heart failure with systolic dysfunction were 6, 22 and 35%, P<0.0001. Unadjusted risk of death from all causes associated with heart failure and preserved systolic function was 3.3 (95% CI 2.8-4.0), and after adjustment for baseline characteristics and left ventricular systolic function in multivariate Cox proportional hazards analysis the risk was 2.1 (95% CI 1.7-2.6), P<0.0001. Congestive heart failure is frequently present in patients with preserved left ventricular systolic function, and is associated with increased risk of in-hospital complications and death following acute myocardial infarction.

Event Rates of Acute Myocardial Infarction and Coronary Deaths in Niigata and Nagaoka Cities in Japan.

Mortality from coronary heart disease in Japan is the among lowest recorded in the industrialized nations; however, little is known about the rate of events including nonfatal cases. A survey of event registration and a review of death certificates was carried out to estimate event rates of acute myocardial infarction (AMI) and coronary deaths in the largest 2 cities of the Niigata prefecture where there are 480,720 residents aged between 15 and 65 years. The definitions for these cardiac events used for the WHO-MONICA project were: (1)'definite AMI', (2) 'possible AMI or coronary death' (not including unclassifiable fatal events), and (3) 'unclassifiable fatal events'. Age-adjusted rates for AMI and coronary deaths (per 100,000/year) according to the registration survey were 54.6 for men and 7.2 for women according to definition 1 and 41.9 for men, and 5.3 for women according to definition 2. When data from the death certificate review were taken into account for the estimation, these rates increased to 80.6 for men and 14.2 for women according to definition 1, and 50.0 for men and 9.0 for women according to definition 2. These estimated rates are considerably lower than those in other industrialized nations surveyed in the WHO-MONICA project, and these findings are consistent with those from other studies conducted in Japan.

Trends in fatal coronary heart disease among people aged 25–74 years in Oita City, Japan, from 1987–1998

Serum cholesterol has been increasing in recent years in Japan. There is concern that risk of coronary heart disease (CHD) may be increasing too, but there is little information on validated fatal CHD trends in the Japanese population. We identified 1,056 deaths from heart disease and other deaths possibly hiding CHD from death certificates of residents aged 25–74 years in Oita City, Japan in 1987–1988, 1992–1993, and 1997–1998 (mean population, 273,000 in 1997–1998). We validated 994 of them by medical record review and physician interviews, classifying them into definite fatal acute myocardial infarction (AMI) and possible fatal AMI or CHD death based on Monitoring Trends and Determinants in Cardiovascular Disease project's criteria. Sudden death was defined to estimate the number of CHD sudden deaths. In men, age-adjusted mortality rates due to validated fatal CHD remained quite stable over 10 years (25.3 per 100,000 [95% CI, 15.0–35.5] in 1987–1988 to 24.2 per 100,000 [95% CI, 16.1–32.3] in 1997–1998). When 50% or all sudden deaths were included as fatal CHD, the rates for men tended to decline. This was due to decreasing out-of-hospital deaths in connection with a declining CHD death rate among men aged 65–74 years, whereas in-hospital CHD deaths were level. In women, the rate of validated fatal CHD was highest in 1992–1993, but the 1997–1998 rate was similar to the 1987–1988 rate. We did not find that fatal CHD rates increased in Oita men and women from 1987–1998. Rather, out-of-hospital fatal CHD tended to decline in Oita men.

Exploring sex differences in case fatality in acute myocardial infarction or coronary death events in the northern Sweden MONICA Project.

To investigate sex differences in reaching diagnosis, medical management and case fatality (CF) in acute myocardial infarction (AMI) in the population aged 35-64 years in northern Sweden. Within the framework of the World Health Organization Multinational Monitoring of Trends and Determinants in Cardiovascular Diseases (MONICA) Project, definite AMI was monitored in people aged 35-64 years from 1989 through 1995 (target population 510 000 in 1991). In a population based coronary register, all coronary events were recorded in nine hospitals in 1989-95. The number of events included in the definite coronary myocardial infarction register was 2483 men and 669 women. On admission, a higher proportion of men with definite AMI had chest pain or ECG changes typical for AMI (P < 0.0001). Disagreement between clinical diagnosis and classification by MONICA criteria occurred more often in women (P=0.008). A significantly higher proportion of men was admitted in the coronary care unit and they were significantly more often treated with thrombolytics, nitroglycerine, beta-blockers, or antiplatelet agents. Women received significantly more diuretics, inotropics or calcium antagonists. Diabetes, conferring a worse prognosis, was more common in women (20 vs. 15%; P=0.003). Prehospital CF was significantly higher in men (24.1 vs. 18.3%; P=0.005), but in patients treated in hospital, the CF was significantly lower in men (12.7 vs. 21.2%; P < 0.001). Total CF was equal in men and women. Several factors contributing to the excess in-hospital CF in women were identified, including greater problems in diagnosis of AMI in women which may be one of the reasons for less intensive treatment in women. Differences in co-morbidity, most notably diabetes and medical treatment between men and women with acute AMI may also have played a part.

Trends in acute coronary heart disease mortality, morbidity, and medical care from 1985 through 1997: the Minnesota heart survey.

Coronary heart disease (CHD) mortality continued to decline from 1985 to 1997. We tabulated CHD deaths (ICD-9 codes 410 through 414) in the Minneapolis/St Paul, Minnesota, area. For 1985, 1990, and 1995, trained nurses abstracted the hospital records of patients 30 to 74 years old with a discharge diagnosis of acute CHD (ICD-9 codes 410 or 411). Acute myocardial infarction (AMI) events were validated and followed for 3-year all-cause mortality. Between 1985 and 1997, age-adjusted CHD mortality rates in Minneapolis/St Paul fell 47% and 51% in men and women, respectively; the comparable declines in US whites were 34% and 29%. In-hospital mortality declined faster than out-of-hospital mortality. The rate of AMI (ICD-9 code 410) hospital discharges declined almost 20% between 1985 and 1995, whereas the discharge rate for unstable angina (ICD-9 code 411) increased substantially. The incidence of hospitalized definite AMI declined approximately 10%, whereas recurrence rates fell 20% to 30%. Three-year case fatality rates after hospitalized AMI decreased consistently by 31% and 41% in men and women, respectively. In-hospital administration of thrombolytic therapy, emergency angioplasty, ACE inhibitors, beta-blockers, heparin, and aspirin increased greatly. Declining out-of-hospital death rates, declining incidence and recurrence of AMI in the population, and marked improvements in the survival of AMI patients all contributed to the 1985 to 1997 decline of CHD mortality in the Minneapolis/St Paul metropolitan area. The effects of early and late medical care seem to have had the greatest contribution to rates during this time period.