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Importance of time to reperfusion on outcomes with primary coronary angioplasty for acute myocardial infarction (results from the Stent Primary Angioplasty in Myocardial Infarction Trial).

The mortality benefit of thrombolytic therapy for acute myocardial infarction (AMI) is strongly dependent on time to treatment. Recent observations suggest that time to treatment may be less important with primary percutaneous transluminal coronary angioplasty (PTCA). Patients with AMI of <12 hours duration, without cardiogenic shock, who were treated with primary PTCA from the Stent PAMI Trial (n = 1,232) were evaluated to assess the effect of time to reperfusion on outcomes. Thrombolysis In Myocardial Infarction grade 3 flow was achieved in a high proportion of patients regardless of time to treatment. Improvement in ejection fraction from baseline to 6 months was substantial with reperfusion at <2 hours but was modest and relatively independent of time to reperfusion after 2 hours (<2 hours, 12.3% vs > or =2 hours, 4.2%, p = 0.004). There were no differences in 1- or 6-month mortality by time to reperfusion (6-month mortality: <2 hours [5.5%], 2 to <4 hours [4.6%], 4 to <6 hours [4.5%], >6 hours [4.2%], p = 0.97). There were also no differences in other clinical outcomes by time to reperfusion, except that reinfarction and infarct artery reocclusion at 6 months were more frequent with later reperfusion. The lack of correlation between time to treatment and mortality in patients without cardiogenic shock suggests that the survival benefit of primary PTCA may be related principally to factors other than myocardial salvage. These data may also have implications regarding the triage of patients with AMI for primary PTCA.

Aged↗

Embolic cerebral infarction and gastrointestinal hemorrhage following thrombolytic therapy for acute myocardial infarction.

We report an unusual case of cerebral embolization that occurred after intravenous thrombolytic therapy for myocardial infarction. Direct observation by serial echocardiograms in this patient confirmed that the thrombolytic treatment induced lysis and fragmentation of thrombus, and the subsequent dislodging and embolization of preexisting cardiac thrombi, which caused the cerebral infarction. It is suggested that an echocardiogram, if instantly available, be performed before considering thrombolytic therapy whenever acute anterior wall myocardial infarction is impressed.

Aged↗

The use of intra-aortic balloon counterpulsation in patients with cardiogenic shock complicating acute myocardial infarction: data from the National Registry of Myocardial Infarction 2.

BACKGROUND: Cardiogenic shock complicating acute myocardial infarction (AMI) remains the leading cause of death in patients hospitalized with AMI. Although several studies have demonstrated the importance of establishing and maintaining a patent infarct-related artery, it remains unclear as to whether intra-aortic balloon counterpulsation (IABP) provides incremental benefit to reperfusion therapy. The purpose of this study was to determine whether IABP use is associated with lower in-hospital mortality rates in patients with AMI complicated by cardiogenic shock in a large AMI registry. METHODS: We evaluated patients participating in the National Registry of Myocardial Infarction 2 who had cardiogenic shock at initial examination or in whom cardiogenic shock developed during hospitalization (n = 23,180). RESULTS: The mean age of patients in the study was 72 years, 54% were men, and the majority were white. The overall mortality rate in all patients who had cardiogenic shock or in whom cardiogenic shock developed was 70%. IABP was used in 7268 (31%) patients. IABP use was associated with a significant reduction in mortality rates in patients who received thrombolytic therapy (67% vs 49%) but was not associated with any benefit in patients treated with primary angioplasty (45% vs 47%). In a multivariate model, the use of IABP in conjunction with thrombolytic therapy decreased the odds of death by 18% (odds ratio, 0.82; 95% confidence interval, 0.72 to 0.93). CONCLUSIONS: Patients with AMI complicated by cardiogenic shock may have substantial benefit from IABP when used in combination with thrombolytic therapy.

Aged↗

Diffuse cerebral symptoms in convalescents from cerebral infarction and myocardial infarction.

In order to evaluate occurrence and cause of a number of diffuse cerebral symptoms (DCS), such as impaired memory, inability to concentrate, emotional instability, irritability, etc., 44 survivors of cerebral infarction (CI) and 40 survivors of myocardial infarction (MI) were seen 6-26 months after onset for psychometric testing and an interview about DCS. Although surprisingly common in both groups, DCS were significantly more frequent in CI patients than in MI patients. 1/2 of the former and 1/3 of the latter complained of 5 or more symptoms. In contrast, a significant difference in test performance was demonstrated in only 1 of 4 tests. There was no significant correlation between the number of DCS and test performance. In both groups, DCS occurrence was independent of age, whereas in the MI group, but not in the CI group, test performance was inversely related to age. In the CI group, DCS occurrence was not significantly related to size or site of the infarction. The results indicate that an organic brain damage cannot be the sole cause of DCS, and it is suggested that some of the symptoms are manifestations of a stress response syndrome provoked by insufficient coping with the consequences of the disease.

Adult↗

[An elderly patients with ventricular aneurysm, thrombus in the aneurysm, and cerebral infarction 10 years after myocardial infarction].

A 75-year-old man had a 26-year history of hypertension and an 18-year history of effort angina pectoris. He suffered acute myocardial infarction at age 61. According to serial echocardiography, the initially hypokinetic segment of the left ventricular apex was transformed to an apical aneurysm over the course of 10 years (at age 71). Ten months later, a transient ischemic attack occurred, despite the administration of aspirin. At age 72, echocardiography revealed a hyperechoic lesion that was suspected to be a thrombus within the aneurysmal cavity. Cerebral infarction (right occipital lobe) occurred 13 years after myocardial infarction, at age 73. After warfarin therapy for 3 months, the thrombus-like echo in the left ventricular aneurysm disappeared.

Aged↗

[Cerebral infarction and myocardial infarction due to cisplatin-containing chemotherapy].

A 33-year-old man was treated for a testicular non-seminoma carcinoma with three different chemotherapeutic agents: bleomycin, etoposide en cisplatin (BEP). During the second course of BEP he experienced two cerebral infarctions and a myocardial infarction at almost the same time. A CT-scan of the brain revealed a subcortical infarction in the left hemisphere. Angiography of the head and neck arteries revealed an almost completely thrombotic left carotid artery. ECG recordings showed signs of transmural ischaemia of the heart and an echocardiogram demonstrated irreversible myocardial damage. The time interval between the chemotherapy and the complications suggests a cisplatin-related cause (such adverse effects are unknown with bleomycin or etoposide). Cisplatin toxicity can give rise to serious vascular complications for which several factors appear to be responsible, such as an increased thrombogenicity and vascular spasm due to hypomagnesaemia.

Adult↗

[Cardiac tamponade as a complication of acute myocardial infarct. (Clinical and pathologico-anatomic analysis of patients with acute myocardial infarct and cardiac tamponade)].

Cardiac tamponade is a frequent cause of death in acute myocardial infarction--in as many 23%. It is encountered in particular in the 7th and 8th decade, in patients with a first infarction which is frequently situated in the anterior wall of the left ventricle. 93% of the patients have obvious ECG manifestations of Q infarction. The diagnosis of cardiac tamponade is easy when during an acute terminal attack slow activity on the ECG tracing is found without a haemodynamic response and the pulse on the great arteries is not palpable even after external cardiac massage. In 80% the onset of cardiac tamponade is very sudden. The presence of shock or cardiac failure makes the diagnosis of cardiac tamponade more difficult. As to investigated indicators, in the development of cardiac tamponade the systemic pressure--systolic as well as diastolic--on admission or during hospitalization, may play a part. The patients have a less marked coronary sclerosis, fibrosis of the cardiac muscle is less frequently present. Previous necroses of the heart muscle may have probably a certain protective effect on the development of cardiac tamponade. Anticoagulants obviously do not influence the development of cardiac tamponade.

Aged↗

L-arginine therapy in acute myocardial infarction: the Vascular Interaction With Age in Myocardial Infarction (VINTAGE MI) randomized clinical trial.

CONTEXT: The amino acid L-arginine is a substrate for nitric oxide synthase and is increasingly used as a health supplement. Prior studies suggest that L-arginine has the potential to reduce vascular stiffness. OBJECTIVE: To determine whether the addition of L-arginine to standard postinfarction therapy reduces vascular stiffness and improves ejection fraction over 6-month follow-up in patients following acute ST-segment elevation myocardial infarction. DESIGN AND SETTING: Single-center, randomized, double-blind, placebo-controlled trial with enrollment from February 2002 to June 2004. PATIENTS: A total of 153 patients following a first ST-segment elevation myocardial infarction were enrolled; 77 patients were 60 years or older. INTERVENTION: Patients were randomly assigned to receive L-arginine (goal dose of 3 g 3 times a day) or matching placebo for 6 months. MAIN OUTCOME MEASURES: Change in gated blood pool-derived ejection fraction over 6 months in patients 60 years or older randomized to receive L-arginine compared with those assigned to receive placebo. Secondary outcomes included change in ejection fraction in all patients enrolled, change in noninvasive measures of vascular stiffness, and clinical events. RESULTS: Baseline characteristics, vascular stiffness measurements, and left ventricular function were similar between participants randomized to receive placebo or L-arginine. The mean (SD) age was 60 (13.6) years; of the participants, 104 (68%) were men. There was no significant change from baseline to 6 months in the vascular stiffness measurements or left ventricular ejection fraction in either of the 2 groups, including those 60 years or older and the entire study group. However, 6 participants (8.6%) in the L-arginine group died during the 6-month study period vs none in the placebo group (P = .01). Because of the safety concerns, the data and safety monitoring committee closed enrollment. CONCLUSIONS: L-arginine, when added to standard postinfarction therapies, does not improve vascular stiffness measurements or ejection fraction and may be associated with higher postinfarction mortality. L-arginine should not be recommended following acute myocardial infarction. Clinical Trial Registration ClinicalTrials.gov, NCT00051376.

Aged↗

Residual flow to the infarct zone against lethal ventricular tachyarrhythmias during the acute phase of myocardial infarction.

BACKGROUND: The benefits of residual flow to the infarct zone have been demonstrated in acute myocardial infarction (AMI), but its relation to ventricular tachyarrhythmias remains uncertain. HYPOTHESIS: This study was undertaken to test the hypothesis that residual flow is an important determinant of lethal ventricular tachyarrhythmias (sustained ventricular tachycardia or ventricular fibrillation) during the acute phase of AMI. METHODS: We investigated the determinants of lethal ventricular tachyarrhythmias within 24 h after the onset of symptoms in 310 consecutive patients (256 men; age 57.4 +/- 11.5 years) with AMI undergoing primary angioplasty. Patients were divided into two groups: those with (Group 1, n = 40) and those without (Group 2, n = 270) lethal ventricular tachyarrhythmias. Residual flow was defined as the presence of anterograde flow (> or = Thrombolysis in Myocardial Infarction [TIMI] 2 flow) or good angiographic collaterals (> or = grade 2) on a preintervention angiogram. RESULTS: Univariate determinants of lethal ventricular tachyarrhythmias were cardiogenic shock, systolic blood pressure, peak level of creatine kinase, culprit artery, spontaneous reperfusion, and residual flow. In multivariate analysis, however, cardiogenic shock (odds ratio [OR] = 4.79, 95% confidence interval [CI] 1.63-14.11, p = 0.004), residual flow (OR = 0.34, 95% CI 0.14-0.81, p = 0.015), and the right coronary artery as the culprit artery (OR = 2.09,95% CI 1.03-4.22, p = 0.040) were independent determinants of these arrhythmias. In-hospital death occurred in 10 patients and was more common in Group 1 than in Group 2 (12.5% vs. 1.9%, respectively, p < 0.001). CONCLUSION: The absence of residual flow was associated with greater risk of lethal ventricular tachyarrhythmias during the acute phase of AMI, suggesting a protective role of residual flow against these arrhythmias in AMI.

Angioplasty↗

The effect of intravenous nitroglycerin on coronary blood flow and infarct size during myocardial infarction in conscious dogs.

Nitroglycerin (TNG), based on electrocardiographic evidence, has been shown to reduce myocardial ischemia, but its effect on morphometrically and enzymatically estimated infarct size has not been defined. Accordingly, coronary occlusion was produced in 50 conscious dogs without LV failure. Twenty-five received TNG (200-300 micrograms/min i.v. for 8 h) and the results compared with those in 25 untreated dogs. Coronary blood flow was measured with 141Ce, 85Sr, and 95Nb (9 microns) after occlusion before TNG, 30 min after TNG, and again at 8 h. Mean blood pressure decreased from 103 to 84 mmHg with TNG vs. 99 to 94 mmHg in controls (p < 0.02). Average heart rates were similar [135 +/- 26 vs. 120 +/- 33 beats/min (SD)]. TNG Did not increase total transmural coronary flow in any region but increased subendocardial flow in the central ischemic areas by 45% (0.09 ml/min/g vs. 0.13 ml/min/g). Animals were sacrificed after 24 h. Infarct size estimated morphometrically (25 +/- 1.5 vs. 26 +/- 1.5 of LV weight) and from myocardial CK depletion (23 +/- 2 vs. 23 +/- 2) was similar for the two groups. Thus, despite increased subendocardial flow, prolonged i.v. TNG did not decrease infarct size even though a difference of 15% would have been detected with this sample size. TNG May relieve coronary spasm but does not appear to be beneficial with sustained coronary occlusion.

Animals↗

Relationship between electrocardiographically estimated infarct size and clinical findings in inferior myocardial infarction.

In 270 patients with acute inferior wall myocardial infarction (MI) and no previous MI, Q- and R-wave changes in leads II, III, and aVF in a 12-lead standard ECG were related to the clinical course during hospitalization and 3-month follow-up. Patients with ECG-defined transmural MI showed a higher incidence of tachycardia, high degree of AV block, congestive heart failure (CHF), and pericarditis than patients with nontransmural MI. In a subgroup including 226 patients, the series was divided into quartiles according to the sum of Q- and R-wave changes in leads II, III, and aVF 4 days after arrival in hospital. A weak correlation between ECG-determined infarct size and the incidence of complications such as congestive heart failure (CHF), need for furosemide, and pericarditis, as well as the duration of hospitalization was observed. It is concluded that ECG-determined infarct size from leads II, III, and aVF in inferior MI is associated with the clinical course, although it cannot predict the outcome in the individual patient.

Adult↗

The relationship between the electrocardiographically estimated infarct size and 1- and 2-year survival in acute myocardial infarction.

In 587 patients with acute myocardial infarction (AMI) and no previous MI, electrocardiographically estimated infarct size was related to 1- and 2-year mortality. The overall mortality was higher in patients with transmural MI (Q- or R-wave changes in standard ECG) than in patients with subendocardial infarction (ST-T-wave changes in standard ECG) after 1 year (18.8% compared to 6.5% p less than 0.001) and after 2 years (22.2% compared to 13.8%, p = 0.049). When patients who were alive during primary hospitalization were analyzed separately, slightly higher mortality was found in patients with transmural MI than in subendocardial MI after 1 year (9.6% compared to 4.2%, p = 0.076) while no difference was found after 2 years (13.4% as compared to 11.7%, p greater than 0.2). In a subgroup of patients with anterior MI, precordial mapping with 24 chest leads was analyzed 4 days after arrival in hospital (n = 197). Patients were divided into quartiles according to the sum of R waves, the sum of Q waves, and the number of Q waves. There was a similar overall mortality in each quartile after 1 year and after 2 years regardless of ECG parameters studied. Neither did we find any correlation between the sum of R waves in leads II, III, and aVF on the fourth day in patients with inferior MI and overall 1- or 2-year mortality rate, although there was a trend towards higher mortality with more ECG changes.

Adult↗

Acute anterior myocardial infarction: streptokinase prevents ventricular thrombosis independently of its effect on infarct size.

Left ventricular thrombosis (LVT) is a frequent complication after acute anterior myocardial infarction (AMI). The purpose of this study is to evaluate whether streptokinase (SK) therapy prevents LVT, and whether this effect is due to the preservation of left ventricular function or to the fibrinolytic action of the drug. Sixty-five patients who underwent a left ventricular angiography within 2 months after a first AMI were studied. Twenty-eight patients (SK group) received SK 1,500,000 U i.v. administered over 60 min within 6 h from the onset of symptoms. A lower incidence of LVT was found in the SK group (p = 0.0003). We divided patients into two classes according to the value of akinetic-dyskinetic area (AD): the first group with a lower value of AD, the second group with a higher value of AD. In both groups, a reduced incidence of LVT was associated with SK therapy (p = 0.014, p = 0.015, respectively). Early infusion of SK during AMI seems to prevent the development of LVT, with an effect partly independent from its action on infarct size for small to large myocardial infarction.

Female↗

Comparison between diurnal distribution of onset of infarction in patients with acute myocardial infarction and circadian variation of blood pressure in patients with coronary artery disease.

We analyzed the diurnal distribution of the onset of infarction in 636 patients with acute myocardial infarction (MI) and compared it with the circadian variation of blood pressure in 57 patients with coronary artery disease (CAD). In addition, we studied the modification of the circadian blood pressure variation during treatment with antianginal medications in 20 patients with CAD. A marked diurnal periodicity (p < 0.05) was observed for the onset of MI, with peaks seen in the late morning, late evening, and very early morning. The blood pressure in the patients with CAD was elevated in the morning, reduced in the late evening, and was the lowest in the very early morning. The peaks of onset of infarction temporally corresponded to the characteristic feature of blood pressure profile observed in the patients with CAD, that is, the morning rise, the late evening decline, and the very early morning reduction. Antianginal medications significantly reduced the blood pressure, not only during the day (p < 0.02) but also at night (p < 0.05). These observations suggest that the decline in blood pressure, as well as the morning surge in blood pressure, may be closely related to the onset of MI. Therefore, when treating patients with CAD with antianginal medications which can potentially reduce blood pressure, the effects on the circadian variation of blood pressure should be considered.

Blood Pressure↗

Long-term prognosis after myocardial infarction: univariate and multivariate analysis of clinical characteristics in 1,000 patients. Kyoto and Shiga Myocardial Infarction (KYSMI) Study Group.

To examine the clinical outcome for patients with myocardial infarction and to analyze clinical predictors for long-term prognosis, 1,000 patients were studied retrospectively. Between January 1983 and December 1987, 1,002 consecutive patients with myocardial infarction, who resided in the Kyoto and Shiga districts, were reviewed after coronary arteriography, but in two patients medical records were not located. During 3.3 +/- 2.0 years, 75 patients died of cardiac causes and 301 experienced cardiac events (death, reinfarction, and revascularization). Overall 5-year cardiac mortality was 8% and cardiac event rate was 35%. Among determinants of age, smoking, hypertension, diabetes mellitus, heart failure, postinfarction angina, serious arrhythmia, mitral regurgitation, digitalis and diuretics administration, ejection fraction (EF), left main trunk disease, and number of diseased coronary arteries selected by univariate analysis, multivariate analysis revealed that heart failure, EF, number of coronary vessel disease, diabetes, and mitral regurgitation were the important predictors of cardiac death. For cardiac events, multivariate analysis demonstrated that the number of diseased coronaries, postinfarction angina, and left main trunk disease were significant predictors. Therefore, impaired left ventricular function and myocardial ischemia appear to be important markers for cardiac death, but impaired left ventricular function does not appear to be a predictor for cardiac events. The data obtained in this study will be useful in the assessment of patients with myocardial infarction and will be of clinical significance in predicting mortality and cardiac events.

Adult↗

The appearance of L-selectin(low) polymorphonuclear leukocytes in the circulating pool of peripheral blood during myocardial infarction correlates with neutrophilia and with the size of the infarct.

BACKGROUND: It is assumed that not only leukocytosis, but also the activation of white blood cells (WBC) may play a role in the pathogenesis and prognosis of patients with myocardial infarction (MI). Activation of WBC includes upregulation of CD11b/CD18 and downregulation of CD62L (L-selectin) antigens. HYPOTHESIS: The activation of WBC is associated with the appearance of a larger MI. METHODS: CD11b/CD18 and CD62L were measured on the surface of WBC on Day 1 and Day 3 from the onset of MI. The size of the infarct with estimated by calculating the area under the curve of the creatine kinase enzyme, which was measured every 6 h. RESULTS: A negative correlation was noted between the absolute polymorphonuclear count and the availability of the CD62L on these cells during Day 1 (r = -0.46, p = 0.003) and Day 3 (r = -0.35, p = 0.05). There was a positive correlation between the size of MI and the WBC count (r = 0.46, p = 0.004) and a negative correlation with CD62L on polymorphonuclears (r = -0.35, p = 0.03). During Day 3, the CD11b/CD18 on the polymorphonuclears increased despite a decrement in the absolute number of these cells. CONCLUSION: The neutrophilia during the early phases of acute MI correspond to the appearance of the L-selectin(low) population of polymorphonuclear leukocytes. There is a correlation between the appearance of this population and the size of the infarct.

Aged↗

[Childhood and myocardial infarct: socioeconomic and psychosocial influences in childhood on risk of myocardial infarct].

OBJECTIVES: Compared to the established risk factors of myocardial infarction (MI) little is known about the impact of socio-economic and psycho-social risk factors during childhood. METHODS: Based on the WHO MONICA infarction register of the Erfurt reporting unit (1990-1993), 129 male cases and 129 controls (patients of accident surgery without psychiatric or heart disease, matched by age groups) were surveyed by a qualitative interview. The MI risk was analysed for general conditions of childhood, stressful life events, serious changes during childhood, and dissatisfaction with childhood using univariate and multiple logistic regression models. RESULTS: A significantly higher risk was found for worse (OR = 5.1; CI: 1.5-18.1) and mediocre (OR = 2.0; CI: 1.0-4.1) housing conditions as well as migration (OR = 3.0; CI: 1.1-8.3) during childhood. A significantly increased risk of MI is also found for individuals who reported three or more stressful life events (OR = 3.2; CI: 1.1-9.4) during childhood. In comparison, smoking habits (current or ex-smokers)--an established impact factor on MI--was associated with a slightly lower risk (OR = 2.6; CI: 1.3-5.3). CONCLUSIONS: Both socio-economic determinants and psycho-social factors of childhood carry significant risk for myocardial infarction in later life. Our data support the hypothesis that risk factors of MI are affected and/or triggered by socio-economic living conditions during childhood in general, and by stressful life events during childhood in particular.

Adult↗

The impact of diabetes mellitus on survival after myocardial infarction: can it be modified by drug treatment? Results of a population-based myocardial infarction register follow-up study.

AIMS/HYPOTHESIS: Mortality of diabetic patients after myocardial infarction remains high despite recent improvement in their management. This study population-based evaluates the impact of cardiovascular drug therapy on mortality within 28 days and during 5-year follow-up in diabetic compared with non-diabetic patients. METHODS: Using the MONICA Augsburg register from 1985 to 1992, 2210 inpatients with incident Q-wave myocardial infarction aged 25-74 years were included, of whom 468 had diabetes. Primary end point was mortality within 28 days and over 5 years. General linear model procedures were used for age-adjustment, controlling for sex, and testing significance; hazard risk ratios were calculated using multivariable Cox proportional hazards model procedures. RESULTS: During the 5-year follow-up, 598 subjects died (396 diabetic, 202 non-diabetic). The mortality rate within 28 days was 12.6% in diabetic patients (women 18.0%, men 9.9%) and 7.3% in non-diabetic patients (p = 0.001). Mortality in diabetic patients over 5 years was increased by 64% (95% confidence interval 1.39-1.95) compared with non-diabetic patients. This was considerably reduced (p < 0.001) in patients treated with thrombolytic drugs (risk ratio: diabetes 0.57, no diabetes 0.65) and with beta blockers (0.62 and 0.64) and antiplatelets (0.76 and 0.74) at hospital discharge. Mortality of diabetic patients treated with these drugs was reduced to that of non-diabetic patients without such treatment (risk ratio 1.01 to 1.27; p > 0.1). CONCLUSION/INTERPRETATION: Diabetic patients after myocardial infarction are at particularly high risk of dying, but benefit clearly from treatment with thrombolytics, beta blockers and antiplatelets. This study does not, however, allow any inferences to be drawn for treatment with angiotensin converting enzyme inhibitors or the impact of left ventricular function.

Adrenergic beta-Antagonists↗