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PubMed1990

Left ventricular volumes in the recovery phase after myocardial infarction: relation to infarct location, left ventricular function and one-year cardiac mortality.

Absolute left ventricular volumes, normalized to body surface area, were determined by a count-based radionuclide technique in 189 patients with myocardial infarction (MI). All examinations were performed in the second week after MI. Fifty-three percent of the patients had an increased end-diastolic volume index (EDVI) and 72% an increased end-systolic volume index (ESVI). Patients with anterior MI had the same median EDVI as patients with inferoposterior MI, but significantly higher median ESVI and significantly lower median stroke volume index (SVI). SVI was subnormal in 19% of the 189 patients and left ventricular ejection fraction (LVEF) was subnormal in 67%. A non-linear, inverse relationship was present between EDVI and LVEF and between ESVI and LVEF, but LVEF varied greatly for any degree of ventricular dilatation. During a 1-year follow-up period, death from cardiac causes occurred in 29 patients. A strong relationship was present between the degree of ventricular dilatation and 1-year mortality, as well as between the degree of SVI or LVEF reduction and 1-year mortality but, next to clinical heart failure, LVEF was the single most powerful predictor of cardiac death, and various combinations of EDVI, ESVI and SVI did not add more prognostic information to that obtained by heart failure than did LVEF.

Aged↗
PubMed1992

Prevalence of transient myocardial ischaemia during the first year after a myocardial infarction. Effect of treatment with verapamil. The Danish Study Group on Verapamil in Myocardial Infarction.

DAVIT-II is a double-blind, randomized, multicentre, placebo-controlled study of long-term treatment with verapamil 360 mg per day administered to patients who have suffered an acute myocardial infarction (AMI). In the present study, comprising a subset of DAVIT-II, 48 h continuous ECG recordings demonstrated transient ST segment deviation indicative of myocardial ischaemia after one week, prior to randomization, in 18% (10 of 57) of the patients. After one month, 24% (11 of 46) of the placebo and 8% (3 of 39) of the verapamil-treated patients (P = 0.04) had myocardial ischaemia; after one year the figures were 26% (9 of 35) and 4% (1 of 27) (P = 0.02), respectively. At 18 months the 'major' event rate in patients who had had ischaemia before randomization was 40% and 23.8% in patients without ischaemia (P = 0.057). In the placebo group, 63% of 91 episodes of ST depression were recorded between 0600 h and 1800 h, and 62% of 26 episodes of ST elevation between 1800 h and 0600 h (P less than 0.001). Nine episodes of ST depression and no episode of ST elevation were recorded in the verapamil-treated patients. In conclusion, 20-25% of post-AMI patients have transient ischaemia; verapamil prevents ischaemia, and a pronounced circadian variation of ST segment deviations can be demonstrated.

Aged↗
PubMed1994

Randomized controlled trial of oral captopril, of oral isosorbide mononitrate and of intravenous magnesium sulphate started early in acute myocardial infarction: safety and haemodynamic effects. ISIS-4 (Fourth International Study of Infarct Survival) Pilot Study Investigators.

The purpose of this randomized controlled study was to assess the haemodynamic effects, safety and tolerability in acute myocardial infarction (AMI) of one month of oral captopril, one month of oral isosorbide mononitrate and 24 h of intravenous magnesium. It was carried out in four United Kingdom and six Polish hospitals in consecutive phases: oral captopril vs oral mononitrate vs placebo were compared among 400 patients in a 'three-way' study; and then oral captopril vs placebo and oral mononitrate vs placebo were compared among 474 patients in '2 x 2' and '2 x 2 x 2' factorial studies (with 208 patients in the latter study also randomized between intravenous magnesium and open control). The factorial studies differed from the three-way study in that one group of patients was allocated both oral captopril and oral mononitrate, a higher maintenance dose of captopril was used (following the same initial dose), and once daily controlled-release mononitrate was used. In the three-way study, the mean of the lowest systolic blood pressures recorded during the first 4 h after randomization were (mmHg +/- standard error): 104 +/- 2 captopril vs 105 +/- 1 mononitrate vs 112 +/- 2 placebo (P < 0.001 for captopril or for mononitrate vs placebo), and in the factorial studies were 105 +/- 1 captopril vs 110 +/- 1 placebo (P < 0.01) and 106 +/- 1 mononitrate vs 108 +/- 1 placebo (NS). There was an excess of hypotension recorded among patients allocated active treatment (captopril > mononitrate > placebo) and there was a small, but significant, excess of cardiogenic shock with captopril compared with control in the factorial study. However, in these studies, neither captopril nor mononitrate were associated with any overall increase in the incidence of hypotension considered severe enough to lead to treatment being stopped. No other serious complications were observed, and compliance with study tablets at hospital discharge was not significantly different between the active and placebo groups. Patients allocated magnesium in the 2 x 2 x 2 factorial study had a slightly lower mean systolic blood pressure just after the initial 15 min bolus injection (126 +/- 2 magnesium vs 134 +/- 3 control; P < 0.05) but there were no significant differences during the subsequent 24 h maintenance infusion period. Apart from some facial flushing, magnesium did not appear to be associated with any complications.(ABSTRACT TRUNCATED AT 400 WORDS)

Captopril↗
PubMed1996

Determinants of infarct size in acute myocardial infarction in patients treated with reperfusion therapy.

Infarct size after reperfusion therapy is determined by the extent of myocardium at risk, the degree of residual blood flow within the jeopardized zone, and the duration of coronary occlusion. This review article will explore the noninvasive methods that have been used to measure these variables. Recent advances in nuclear cardiology techniques will be discussed in detail, because new agents have the ability to accurately quantify these variables.

Clinical Enzyme Tests↗
PubMed1994

Intravenous metoprolol preceding thrombolysis in acute thrombotic myocardial infarction in the dog; effects on infarct size, myocardial blood flow, and left ventricular function.

Intravenous (i.v.) metoprolol preceding thrombolysis in an anesthetized dog model of thrombotic occlusion of the anterior descending coronary artery helps limit infarct size (IS). We wished to determine whether these effects are caused at least in part by enhancement of collateral blood flow to the area at risk (AAR). Thrombotic occlusion was provoked by a copper-coil technique. We measured intracardiac pressures and their derivatives by catheter-tip micromanometers, cardiac output (CO) by thermodilution method, regional myocardial blood flow (RMBF) by radioactive microspheres technique, global and regional left ventricular (LV) function by ventriculography, and IS with triphenyltetrazolium at the end of the experiment. Measurements were performed before and after 60-min occlusion and after 30- and 90-min reperfusion. Received fifteen minutes after occlusion, 12 dogs metoprolol 0.3 mg/kg i.v. followed by 0.3 mg/kg/h; 12 received saline. Thrombolysis was performed in all dogs after 60-min occlusion with recombinant tissue-type plasminogen activator (rt-PA) 10 micrograms/kg/min for 30 min. Hemodynamic findings were similar in both groups. During occlusion, collateral flow to total AAR (18.6 +/- 7.5 vs. 11.0 +/- 6.1 ml/min/100 g), to its subepicardial (22.1 +/- 8.1 vs. 12.2 +/- 7.2 ml/min/100 g), midmyocardial (16.0 +/- 8.9 vs. 8.0 +/- 5.5 ml/min/100 g), and endocardial (14.1 +/- 8.1 vs. 7.3 +/- 6.0 ml/min/100 g) layers was higher (p < or = 0.03) in metoprolol than in placebo-treated dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1998

New Q waves do not always a new infarct spell: right bundle branch block-dependent Q waves simulating infarct extension.

We present the electrocardiograms of three patients, representative of 14, with acute anterior wall infarction in whom, in contrast to current understanding, the appearance of right bundle branch block was associated with a shift of the initial vector of depolarization that resulted in 'new' Q waves in V1-V2 that mimicked extension of necrosis. This little-known electrocardiographic phenomenon should be kept in mind when consideration is given to attempts at reperfusion.

Aged↗
PubMed2001

Changes in the use of medications after acute myocardial infarction: possible impact on mortality after myocardial infarction and long-term outcome.

OBJECTIVE: To describe the change in the use of medication after acute myocardial infarction (AMI) and discuss its possible impact on risk and risk indicators for death. PATIENTS: All patients discharged alive after hospitalization for AMI at Sahlgrenska Hospital (covering half the community of Göteborg, i.e. 250,000 of 500,000 inhabitants) during 1986-1987 (period I) and at Sahlgrenska Hospital and Ostra Hospital (covering the whole community of Göteborg, 500,000 inhabitants) during 1990-1991 (period II). METHODS: Overall mortality was retrospectively evaluated during 5 years of follow-up. RESULTS: In all, 740 patients were included in the study during period I and 1448 during period II. The 5-year mortalities were 44.1% for period I patients and 39.3% for period II patients (P = 0.036). The relative risk of death for period II patients was 0.78 [95% confidence interval (CI) 0.67-0.89, P = 0.0005] after adjustment for differences at baseline. There was a significant interaction with a history of congestive heart failure; improvement in duration of survival was found only for patients without such a history. During period I, only 3% of patients were administered fibrinolytic agents, compared with 33% of patients during period II (P < 0.0001). During period I, aspirin was prescribed for 13% of patients discharged from hospital compared with 79% during period II. Other changes in treatment on going from period I to period II included increases in prescription of beta-blockers and angiotensin converting enzyme inhibitors. After adjustment for various risk indicators for death, relative risk of death for those administered fibrinolytic agents was 0.60 (95% CI 0.18-2.02) for patients in the period-I cohort and 0.68% (95% CI 0.51-0.91) for those in the period-II cohort. Adjusted relative risk of death for those prescribed aspirin upon discharge from hospital was 0.81 (95% CI 0.52-1.25) for period-I patients and 0.71 (95% CI 0.56-0.91) for period-II patients. The adjusted relative risk of death for those administered beta-blockers was 0.72 (95% CI 0.55-0.96) for period-I patients and 0.70 (95% CI 0.55-0.90) for period-II patients. CONCLUSION: Increased use of fibrinolytic agents and aspirin for AMI as well as a moderate increase in use of beta-blockers and angiotensin converting enzyme inhibitors was associated with a parallel reduction in age-adjusted mortality during the 5 years after discharge from hospital. However, this improvement was seen only for patients without histories of congestive heart failure.

Adult↗
PubMed1984

Relationship between enzymatically estimated infarct size and short- and long-term survival after acute myocardial infarction.

In 585 patients with acute myocardial infarction (AMI) and no previous MI the maximal activity of serum heat-stable lactate dehydrogenase (LD) (EC 1.1.1.27) activity was related to 1-year and 2-year mortality rates. All patients participated in a double-blind trial with metoprolol during the first three months after an AMI. Thereafter both groups were treated in a similar way. A strong relationship was found between LD maximum activity and the in-hospital prognosis (p less than 0.001), the 1-year survival rate (p less than 0.001) and the 2-year survival rate (p less than 0.001). When the patients who were alive after primary hospitalization were analyzed as a separate group, the relationship between LD maximum activity and 1-year and 2-year survival rates remained (p less than 0.001). In a subsample of 171 patients the maximal activity of creatine kinase (CK) (EC 2.7.3.2) and CK subunit B did not correlate either with in-hospital, 1-year or 2-year survival rates. We conclude that, when a sufficiently large number of patients are investigated, there is a strong relationship between serum enzyme maximum activity and short- and long-term survival.

Adult↗
PubMed1991

Thalassaemia trait and myocardial infarction: low infarction incidence in male subjects confirmed.

A total of 4401 subjects admitted to the Medical Division of St Camillo Hospital in Comacchio (Ferrara, Italy) over a period of 7 years were prospectively evaluated in order to determine whether the heterozygous beta-thalassaemic (HBT) could be considered as a protective factor against the occurrence of acute myocardial infarction (AMI). Of the total patient sample, 3954 subjects were non beta-thalasaemics (NBTs), and 447 subjects were heterozygous beta-thalassaemics (HBTs). AMI was diagnosed in 384 patients, of whom 17 individuals were HBTs and 367 subjects were NBTs. The prevalence of HBTs in this group was significantly lower than expected (4.43%, P less than 0.0001). Furthermore, an analysis by sex showed that this lower prevalence could be attributed to male patients. Moreover, only in male subjects was a significant negative correlation observed between AMI and HBT. The mean age at which AMI occurred in male HBTs was significantly higher than in male NBTs (72 +/- 2.69 vs. 63 +/- 0.7 years, P less than 0.05), while no differences were found in the mean age at which AMI occurred between HBT and NBT female subjects. This study demonstrates that the thalassaemic trait may afford some protection against the occurrence of AMI in men.

Aged↗
PubMed2005

Favourable trends in the incidence and outcome of myocardial infarction in nondiabetic, but not in diabetic, subjects: findings from the MONICA myocardial infarction registry in northern Sweden in 1989-2000.

BACKGROUND: The aim of this study was to compare time trends in incidence, case fatality and mortality due to myocardial infarction (MI) in patients with or without diabetes. METHODS: This study was based on the Northern Sweden MONICA Project MI registry with a target population of about 200,000 inhabitants in the age group 35--64 years in the two northernmost counties of Sweden. During 1989--2000, 6254 patients who had had an MI according to MONICA criteria were included in this study: 4569 patients had a first MI and 1685 had a recurrent MI. Sixteen per cent of the men and 20% of the women had had diabetes mellitus diagnosed prior the MI. RESULTS: Over the 12-year period, there was a declining trend in incidence and case fatality in first MI. Also, the event rates (first ever and recurrent MI) declined in men without diabetes. In women without diabetes favourable time trends were seen in first ever MI, recurrent MI and in case fatality. There were no favourable time trends for any of these outcomes in patients with diabetes. CONCLUSION: In nondiabetic subjects below the age of 65, the incidence of, and case-fatality in, MI declined. This led to a decreased mortality over the 12-year period. These favourable trends over time were not observed in diabetic subjects.

Adult↗
PubMed2005

Why do acute myocardial infarction patients not call an ambulance? An interview with patients presenting to hospital with acute myocardial infarction symptoms.

BACKGROUND: Studies from overseas indicate that patients with acute myocardial infarction (AMI) symptoms often fail to use the emergency services as recommended, thereby depriving themselves from life-saving treatment in case of cardiac arrest and delaying the time to myocardial reperfusion in the presence of a coronary occlusion. AIMS: To compare patients brought in by ambulance to those not brought in by ambulance and to question why some patients do not use the emergency services when presenting to hospital with AMI symptoms. METHODS: Prospective interview and follow up of consecutive patients presenting with AMI symptoms to the emergency department of a tertiary hospital in a metropolitan area within a 1-month period. RESULTS: Of the 215 patients presenting to the emergency department, 113 (53%) arrived by private transportation. Sixty (53%) of these felt their symptoms did not warrant calling the ambulance, 17 (15%) had first consulted their general practitioner. The private transport group accounted for 28% of documented AMI. CONCLUSIONS: A large proportion of patients with AMI symptoms refrain from calling the emergency services because they do not consider themselves critically ill. Education programmes appear to be warranted because more appropriate use of emergency services will save lives.

Ambulances↗
PubMed1995

Association of silent myocardial ischemia with new atherothrombotic brain infarction in older patients with extracranial internal or common carotid arterial disease with and without previous atherothrombotic brain infarction.

OBJECTIVE: To correlate silent myocardial ischemia with the incidence of new atherothrombotic brain infarction (ABI) in older patients with 40 to 100% extracranial carotid arterial disease (ECAD) with and without prior ABI. DESIGN: In a prospective study of 208 older patients with 40 to 100% ECAD diagnosed by carotid duplex ultrasonography, 24-hour ambulatory electrocardiograms were obtained to detect silent myocardial ischemia. At 42-month mean follow-up, silent myocardial ischemia was correlated with the incidence of new ABI in patients with and without prior ABI. SETTING: A large long-term health care facility where 208 older patients with 40 to 100% ECAD and technically adequate 24-hour ambulatory electrocardiograms for detecting silent myocardial ischemia were studied. PATIENTS: The 208 patients included 68 men and 140 women, mean age 81 +/- 8 years (range 60 to 100). One-hundred three (50%) of the patients had prior ABI. MEASUREMENTS AND MAIN RESULTS: Sixty-nine (33%) of the 208 patients had silent myocardial ischemia. Mean follow-up was 42 +/- 25 months (range 3 to 101 months). At follow-up, the incidence of new ABI was 64% in patients with prior ABI and 32% in patients with no prior ABI (P < .0001). At follow-up, the incidence of new ABI was 65% in patients with silent ischemia and 40% in patients with no silent ischemia (P = .0005). The multivariate Cox regression model showed that patients with prior ABI have a 2.5 times higher chance of developing new ABI than those without prior ABI after controlling other prognostic variables. Patients with silent ischemia have a 2.1 times higher probability of developing new ABI than those without silent ischemia after controlling other prognostic variables. CONCLUSIONS: Prior ABI and silent ischemia are independent risk factors for the development of new ABI in patients with 40 to 100% ECAD. This probably reflects that silent ischemia is a marker for more advanced or more significant atherosclerotic disease rather than a causal factor for ABI.

Aged↗
PubMed2006

Right ventricular infarction mimicking anterior infarction.

It is rare to observe ST elevation in anterior derivations caused by right ventricular branch occlusion. We described the case of a patient with unstable angina who developed acute right ventricular myocardial infarction with ST-segment elevation in anterior precordial leads (V(1)-V(4)) shortly after coronary angiography. Coronary angiogram revealed total occlusion of the right coronary artery (RCA) proximally to the right ventricular branch. This reminds us that the presence of diffuse ST-segment elevation in the precordial leads could be due to acute RCA occlusion. The differentiation of these two entities is important, as their therapies are quite different.

Angina, Unstable↗
PubMed2005

Myocardial viability assessed by dobutamine stress echocardiography predicts reduced mortality early after acute myocardial infarction: determining the risk of events after myocardial infarction (DREAM) study.

OBJECTIVE: To establish further the role of dobutamine stress echocardiography (DSE) in prognostication of outcome early after acute myocardial infarction (AMI) METHODS: Consecutive patients presenting with AMI were screened for inclusion into the study. 212 stable consenting patients underwent DSE a mean (SD) of 4.8 (1.5) days after AMI. Patients were then followed up for 803 (297) days. RESULTS: The mean (SD) resting systolic wall thickening index (SWTI) was 1.6 (0.4), 44% patients had evidence of viability at low dose, and 38% had evidence of ischaemia. During the follow up period 27 (13%) patients died and 16 (8%) had a non-fatal AMI. Independent predictors of both mortality and combined mortality and non-fatal AMI were age (hazard ratio (HR) 1.04/year, p = 0.01, and HR 1.03/year, p = 0.04, respectively) and SWTI at low dose (HR 3.6, p < 0.01, and HR 2.5, p = 0.02, respectively). Low dose DSE provided incremental information over clinical and resting left ventricular function data for predicting death and non-fatal AMI. For patients who were not revascularised SWTI at peak dose dobutamine was the only independent predictor of mortality. CONCLUSION: DSE is a powerful predictor of outcome in stable survivors of AMI. The presence of myocardial viability has a positive impact on survival.

Echocardiography, Stress↗
PubMed1994

Assessment of reperfusion of the infarct zone after acute myocardial infarction by serial cardiac troponin T measurements in serum.

BACKGROUND: The purpose of this study was to derive indices of reperfusion and non-reperfusion after acute myocardial infarction (AMI) from changes in serum concentrations of cardiac troponin T and to test the predictive value of these indices. METHODS: The indices were derived from a retrospective analysis of changes in serum troponin T concentration in 71 patients given thrombolytic treatment who had immediate and late angiography (group 1). These troponin T indices were first tested in a blinded and prospective study of 53 consecutive patients eligible for thrombolytic therapy (group 2). They were then used for the non-invasive assessment of reperfusion of AMI in 48 patients (group 3). RESULTS: In group 1 troponin T serum concentration curves were biphasic in patients who had reperfusion < or = 5.8 h after the onset of symptoms. Release of the cytosolic troponin T pool resulted in a peak at 14 h and ended at 38 h. The probability of reperfusion was > 95% when the ratio of peak cytosolic troponin T concentration to concentration at 38 h (PV1/38) exceeded 1.42 or the ratio of troponin T concentration at 14 h to that at 38 hours (14/38) exceeded 1.09. The probability of the presence of non-reperfused AMI was < 5% when troponin T PV1/38 and 14/38 ratios were < 0.99 and < 0.84 respectively. These discriminatory values of troponin T indices correctly classified (efficiency 96%) 48 of the 53 group 2 patients in whom immediate and late angiography were performed. When troponin T indices were used to classify 48 group 3 patients who were not studied by immediate angiography, thrombolytic therapy was deemed to have been successful in 82% of the treated patients, with spontaneous recanalisation in 11% and 23% of the non-treated patients assessed by PV1/38 and 14/38 respectively. CONCLUSION: The PV1/38 or 14/38 ratios of serum troponin T concentration indicated the effectiveness of thrombolytic therapy in achieving reperfusion of AMI.

Aged↗
PubMed2005

Aphasia following striatocapsular infarction may be explained by concomitant small cortical infarct on diffusion-weighted imaging.

BACKGROUND: The underlying mechanism of aphasia following striatocapsular infarction (SCI) remains controversial. We hypothesized that aphasia resulting from SCI might be associated with concomitant cortical lesions, which can be demonstrated by diffusion-weighted imaging (DWI). METHODS: We analyzed 24 patients with left SCI who underwent DWI and MR angiography within 2 days after the onset. Aphasia was assessed by the modified Korean version of the Boston Diagnostic Aphasia Examination test. RESULTS: DWI showed the presence of additional ischemic lesions involving the cortical areas in 13 of 24 SCI patients (54%). Ten patients (42%) showed aphasia. All 10 patients with aphasia had cortical lesions in addition to SCI (p = 0.0002), whereas 21% (3/14) of the nonaphasic patients had additional cortical lesions. Conventional MRI did not reveal the presence of corresponding acute cortical lesions in any of the aphasic patients. There was no difference between the patients with and without aphasia in terms of their stroke etiology. CONCLUSIONS: Our data suggest that aphasia due to SCI in the acute stage may be attributed to direct cortical injury, whose presence can be demonstrated by DWI, even though it might be invisible on conventional imaging.

Aged↗
PubMed1994

Patients with suspected acute myocardial infarction and acute heart failure: does it matter whether an infarction was developed or not?

Symptoms of acute severe congestive heart failure always raise the suspicion of acute myocardial infarction (AMI). Our aim was to describe the characteristics and the prognosis among patients with acute severe congestive heart failure in relation to whether or not it was caused by AMI. Consecutive patients admitted to one single hospital during 21 months due to suspected AMI, who either had initial symptoms of acute severe congestive heart failure or developed such symptoms during the subsequent days, were prospectively followed for 1 year in terms of mortality and morbidity. Of 531 patients who fulfilled previously defined criteria for severe congestive heart failure, 40% developed AMI during the first 3 days in hospital. At baseline, these patients differed from the others, having a less frequent history of known congestive heart failure. Mortality during 1 year of follow-up was 47% among patients who developed AMI versus 38% among those who did not (p < 0.05). In addition to age and a history of diabetes, development of AMI was independently associated with death.

Adult↗