Sublabial, transseptal, transsphenoidal approach to the pituitary region guided by the ACUSTAR I system

Myocardial infarction occurring in young people with angiographically normal coronary arteries is well described but the pathophysiology of this condition remains unknown. Coronary artery spasm in association with thrombus formation and minimal atheromatous disease or spontaneous coronary artery dissection are possible causes. Two young men presented with severe chest pain after acute alcohol intoxication and each sustained an extensive anterior myocardial infarction. Investigations including intravascular ultrasound showed no evidence of atherosclerotic coronary artery disease. Coronary artery spasm associated with acute alcohol intoxication as well as prothrombotic state and endothelial damage related to cigarette smoking may be mechanisms leading to acute myocardial infarction in these cases. Acute myocardial infarction occurs in young persons with normal coronary arteries and the diagnosis should be considered in young patients presenting with severe chest pain, particularly those abusing cocaine or alcohol, so that reperfusion therapy can be initiated promptly.     

Thoracic pain

A 28-year-old male patient was admitted to our outpatient clinic because of severe chest pain. Past history, ECG and laboratory findings revealed an anterior myocardial infarction and rhabdomyolysis after cocaine consumption. Coronary arteriography performed six days after the infarction showed no significant stenoses. In view of these findings a coronary vasospasm due to cocaine was postulated. Cocaine effects are discussed.     

Myocardial infarct in the puerperium

Two women of 34 and 31 years suffered an acute myocardial infarction in the puerperium. One of them had many risk factors for atherosclerosis: hypercholesterolaemia, hypertriglyceridaemia, diabetes mellitus, hypertension, obesity, nicotine abuse and a positive family history for cardiovascular disease. She had an occluded right coronary artery and was successfully treated with percutaneous transluminal coronary angioplasty. The other patient had an acute myocardial infarction after her first delivery. She was known with hypercholesterolaemia, obesity and nicotine abuse. During her latest pregnancy she was treated with acetylsalicylic acid. Again she developed an acute myocardial infarction in the puerperium, probably due to coronary dissection. Although the incidence of acute myocardial infarction is low in the peripartal period (less than 1 in 10,000) the diagnosis should be considered when a woman presents with chest pain or dyspnoea.     

Acute myocardial infarction in two adolescent males

Acute myocardial infarction in previously healthy children is rare in the absence of congenital anomalies. We describe two cases of acute anterior myocardial infarction in adolescent males with no congenital heart disease, without prior history of or risk factors for coronary heart disease, and with no history of drug abuse. These cases illustrate that myocardial infarction in the absence of systemic illness or coronary anomalies can occur in an adolescent population.     

Incidence of right ventricular asynergy in patients with coronary artery disease

The effects of coronary artery disease on patterns of left ventricular contractility have been thoroughly investigated. In contrast, little is known about the incidence of right ventricular dysfunction induced by this disease. To evaluate the frequency of right ventricular asynergy, biplane right ventricular cineangiograms were obtained in 26 patients. Seven segmental axes of shortening were analyzed in each end-systolic and end-diastolic frame and normalized as percent decrease (or increase) in axis from end-diastolic length. Of 26 patients, 8 (Group I) served as normal (control) subjects. The remaining 18 patients had significant coronary artery disease; 6 of these (Group II) had no significant disease of the right coronary artery, whereas 12 (Group III) had significant obstruction of this artery. Four patients in Group II had a previous anteroseptal myocardial infarction, and six in Group III had a previous inferior myocardial infarction. There was a progressive decrease in segmental axes of shortening from Group I to II and from Group II to II, but the decrease was not significant at the level P less than 0.01. Only one patient in Group II had frank dyskinetic segmental motion of the interventricular septum (this patient had had a previous anteroseptal myocardial infarction), whereas two patients in Group III had dyskinetic segmental motion of the free right ventricular wall (both had previous inferior myocardial infarction). Therefore, coronary artery disease seldom produces significant right ventricular asynergy. Abnormal septal motion is associated with previous anteroseptal myocardial infarction; however, dyskinetic motion of the free right ventricular wall occurs only in patients with a right coronary arterial lesion and previous inferior myocardial infarction.     

Subendocardial myocardial ischemia as assessed with myocardial contrast echocardiography in patients with ischemic heart diseases

Myocardial contrast echocardiography was used to characterize changes in the regional and transmural myocardial blood flow distribution that were provoked by rapid atrial pacing stress in patients with coronary artery diseases. In patients with coronary organic stenosis, a decrease in the myocardial contrast-enhancement in the subendocardial half after rapid atrial pacing was associated with stress-induced chest pain and electrocardiographic ST-T changes. The decrease in the myocardial contrast-enhancement in the subendocardial half after rapid atrial pacing was not observed in patients without coronary stenosis or after coronary angioplasty. Thus, the finding was considered to reflect myocardial ischemia. Pacing-induced decreases in myocardial contrast-enhancement were observed in some patients with old myocardial infarction and significant resting coronary collaterals. In these patients, myocardial ischemia was considered to have developed at rapid pacing because collateral function was good enough to perfuse the infarct myocardium at rest, but was not good enough to prevent myocardial ischemia at stress. Thus, myocardial contrast echocardiography seems to be particularly useful in assessing myocardial ischemia at stress due to coronary stenosis in patients with angina pectoris and due to poor dynamic collateral function in patients with old myocardial infarction.     

In vivo antinociceptive activity of anti-rat mGluR1 and mGluR5 antibodies in rats

Conflicting results of an association between the human platelet antigen 1b (HPA-1b or PlA2) allele and the risk of myocardial infarction and coronary artery disease have been reported. To assess the reason for this discrepancy, we determined the HPA-1 genotype in 298 men who had undergone coronary angiography, including 124 individuals with myocardial infarction, 83 individuals with coronary artery disease but no history of myocardial infarction, and 91 control patients. Among patients with acute or recent onset myocardial infarction (< 1 year), the prevalence of HPA-1b was higher than among patients with coronary artery disease but without myocardial infarction (33 percent vs. 14 percent, p = 0.016). In patients under 60 years of age this difference was even more pronounced (45 percent vs. 15 percent, p = 0.003). Unlike conventional risk factors HPA-1b does not represent a risk factor for coronary artery disease itself but appears to be associated with increased platelet thrombogenicity.     

Social networks and coronary heart disease among Japanese men in Hawaii

A group of 4653 men of Japanese ancestry living in Hawaii were studied for the association of measures of social networks with both the prevalence and incidence rates of coronary heart disease (Honolulu Heart Program, 1971-1979). Prevalence rates for myocardial infarction, angina, and total coronary heart disease were inversely associated with the social network scales in bivariate analyses with age, and in multivariate analyses including 12 other risk factors. With the incidence data, the associations were less evident. Bivariate analysis with age revealed inverse associations for nonfatal myocardial infarction and total coronary heart disease with only one of the social network scales. With multivariate analyses, there was no significant association of any subgroup of coronary heart disease with any scale, although there was a borderline association (p = 0.08) of nonfatal myocardial infarction with one scale. No individual question was significantly associated with either prevalence or incidence rates for coronary heart disease. There was also little evidence of reduced risk of incident coronary heart disease associated with the social network scale for men in high risk categories of serum cholesterol, blood pressure, and cigarette smoking.     

Clenbuterol and anabolic steroids: a previously unreported cause of myocardial infarction with normal coronary arteriograms

During the last 10 years, several cases of myocardial infarction associated with anabolic steroid use have been reported. Postulated mechanisms to explain this association have included changes in lipid levels, the fibrinolytic system, and platelet aggregation. Clenbuterol is a beta 2-agonist with anabolic properties that has not been seen previously with myocardial infarction. We report a case of myocardial infarction in an otherwise healthy 26-year-old body-builder who recently used clenbuterol and anabolic steroids. In this case, synergistic effects of the two agents seem likely to have played a role in the infarct. The normal coronary arteriograms before any anticoagulant or thrombolytic therapy strongly suggest coronary spasm as the mechanism of the infarct.     

Arrhythmias associated with acute myocardial infarction and thrombolysis

Ninety percent of patients with acute myocardial infarction have some cardiac rhythm abnormality, and approximately twenty-five percent have cardiac conduction disturbance within 24 hours following infarct onset. Almost any rhythm disturbance can be associated with acute myocardial infarction, including bradyarrhythmias, supraventricular tachyarrhythmias, ventricular arrhythmias, and atrioventricular block. With the advent of thrombolytic therapy, it was found that some rhythm disturbances in patients with acute myocardial infarction may be related to successful coronary artery reperfusion. This article addresses the role and treatment of arrhythmias and conduction disturbances that complicate the course of patients with acute infarction and thrombolysis.     

The effects of thermogenic agents on hindlimb oxygen consumption in the dog: ICI D7114 and noradrenaline

OBJECTIVES: The purpose of this study was to test the hypothesis that the diameter of the recipient coronary artery of the well developed collateral circulation in patients with acute myocardial infarction increases because of the augmented intravascular pressure caused by subsequent collateral development. BACKGROUND: It is well known that collateral circulation develops after acute myocardial infarction. However, some patients have a well developed collateral circulation at the onset of infarction, which may limit the angiographic evaluation of further development of collateral circulation. METHODS: We measured the diameter of the donor and recipient arteries of the collateral circulation by means of a computer-assisted analysis system in seven patients with acute myocardial infarction who had a totally occluded infarct-related coronary artery during the acute and chronic stages of infarction. All coronary angiograms were obtained after the administration of sublingual nitroglycerin. The measurement was repeated immediately after (within 6 h) and late after (42 +/- 11 days) the onset of acute myocardial infarction. RESULTS: The diameter of the donor artery remained unchanged (1.32 +/- 0.98 vs. 1.42 +/- 1.12 mm). In contrast, the diameter of the recipient artery increased from 1.25 +/- 0.63 to 1.55 +/- 0.61 mm (p < 0.01). These changes in coronary artery diameter were associated with an improvement in regional myocardial wall motion at rest in infarct areas (6.7 +/- 7.0% vs. 13.6 +/- 10.7%, p < 0.05). CONCLUSIONS: These findings indicate that serial measurement of coronary artery diameter is useful for the evaluation of collateral development after acute myocardial infarction.     

The differing prognostic utility of exercise radionuclide ventriculography in coronary artery disease patients with and without prior myocardial infarction

Previous studies have documented the prognostic utility of left ventricular ejection fraction response to exercise primarily in populations without prior myocardial infarction. We undertook a study to assess the prognostic utility of exercise left ventricular ejection fraction and segmental wall motion response during exercise radionuclide ventriculography in coronary artery disease patients with and without prior myocardial infarction. METHODS: We examined the comparative prognostic utility of left ventricular ejection fraction and segmental wall motion response during upright bicycle exercise radionuclide ventriculography in 419 coronary artery disease patients with (n = 217) and without (n = 202) prior myocardial infarction using univariate and multivariate hierarchical regression analyses. RESULTS: During an average followup period of 61 months, 96 patients (23%) suffered cardiac events, including 55/217 (25%) of the patients with prior myocardial infarction and 41/200 (21%) of the patients without prior myocardial infarction (p = ns). Both cumulative Kaplan-Meier survival analyses and stepwise hierarchical Cox survival analyses demonstrated that peak left ventricular ejection fraction < 55% was a significant predictor of cardiac events in patients without prior myocardial infarction (p = 0.04), whereas an exercise wall motion worsening score > or = 2 was a significant predictor in patients with a prior myocardial infarction (p = 0.0001). CONCLUSIONS: The prognostic utility of exercise radionuclide ventriculography variables differ according to the presence or absence of prior myocardial infarction. Global function, assessed by peak left ventricular ejection fraction, adds the greatest prognostic information in patients without prior myocardial infarction, whereas regional function, assessed by exercise wall motion worsening, is the best predictor among patients with prior myocardial infarction.     

Are coronary-care unit changes in therapy associated with improved survival of elderly patients with acute myocardial infarction?

OBJECTIVE: To determine whether changes in coronary-care unit therapy for elderly patients with acute myocardial infarction have been associated with improved survival. MATERIAL AND METHODS: We conducted a retrospective cohort analysis of all patients 70 years of age or older from Olmsted County, Minnesota, who were hospitalized in a coronary-care unit in this county for the treatment of acute myocardial infarction during one of three periods: 1976 through 1978, 1987 through 1989, and 1991. The effect of aspirin, heparin, beta-blockers, thrombolysis, percutaneous transluminal coronary angioplasty, and coronary artery bypass grafting on these elderly patients with acute myocardial infarction was assessed. RESULTS: Improvement in 30-day survival was significant for patients 80 years of age or older (45%, 69%, and 78% in 1976 through 1978, 1987 through 1989, and 1991, respectively; P = 0.01 for the trend) but not for patients 70 to 79 years of age (77%, 76%, and 81% for the three time periods, respectively; P = 0.65 for the trend). The opposite pattern was observed for survival in the period more than 30 days after the event. More intensive treatment in the hospital was associated with better 30-day survival (P < 0.0001). CONCLUSION: The improved survival of the elderly patients with acute myocardial infarction in these cohorts can be accounted for by changes in the therapy they received in the coronary-care units.     

Anabolic steroid abuse and cardiac death

OBJECTIVE: To examine the relationship between anabolic steroid abuse and cardiac death. We report the first two cases in Australia. They are the only reported cases in which the anabolic steroid oxymesterone has been detected. This compound has never been approved for use in Australia. CLINICAL FEATURES: Two footballers, aged 18 and 24, sustained fatal cardiac arrests while at training sessions. Both were considered fit and healthy. OUTCOME: Autopsy revealed features of a hypertrophic cardiomyopathy in the 18-year-old; the 24-year-old had findings of a myocarditis. In both cases the coronary arteries were normal and there was no evidence of coronary thrombosis. Urine in both subjects contained the anabolic steroid oxymesterone. CONCLUSIONS: There are limited clinical uses for anabolic steroids but they are widely abused by athletes in attempts to alter lean body mass and strength. Acute non-fatal myocardial infarction was first reported in 1988 and fatal myocardial infarction in 1990. While a causal relationship is hard to prove, it is possible that the anabolic steroid contributed to the increase in cardiac size in the first subject and may have increased his responsiveness to catecholamines causing an arrhythmogenic event. In the second, the inflammatory changes could have provided the focus for an arrhythmia. It would appear that anabolic steroid abuse should be considered in any athlete presenting with an acute vascular event.     

Myocardial infarction in an adult resulting from coronary aneurysms previously documented in childhood after an acute episode of Kawasaki's disease

Coronary aneurysms resulting from a previous episode of Kawasaki's disease are considered an important cause of myocardial infarction in children. A case of a 19-year-old man presenting with an acute myocardial infarction associated with coronary aneurysms is described. These coronary lesions were previously evaluated angiographically and echocardiographically at the age of 13 years, 5 months after the acute episode of a Kawasaki's disease.     

Sudden coronary death. Frequency of active coronary lesions, inactive coronary lesions, and myocardial infarction

BACKGROUND: The reported frequency of active coronary lesions (plaque rupture and coronary thrombosis) in sudden death due to coronary artery atherosclerosis (sudden coronary death) has varied from < 20% to > 80% of cases in previous series. In hearts lacking an active coronary lesion, sudden death has usually been attributed to a healed myocardial infarction. The purpose of the present study was to determine the frequency of active and inactive coronary lesions and myocardial infarction in individuals with sudden coronary death. METHODS AND RESULTS: The hearts of persons who died as a result of sudden coronary death underwent perfusion-fixation and postmortem angiography. An active coronary lesion was defined as a disrupted plaque, luminal fibrin/platelet thrombus, or both. We defined an inactive lesion as having a cross-sectional luminal stenosis of > or = 75% with neither plaque disruption nor luminal thrombus. Ninety hearts were examined (from 72 men and 18 women; mean age at the time of death, 51 +/- 10 years). Acute myocardial infarction was present in 19 (21% [acute myocardial infarction only in 9, both acute and healed myocardial infarction in 10]), healed myocardial infarction only in 37 (41%), and no myocardial infarction in 34 (38%). Active coronary lesions were identified in 51 (57%): acute thrombi plus disrupted plaques in 27, acute thrombi only in 21, and disrupted plaques only in 3. In hearts with acute myocardial infarction, active coronary lesions were significantly more prevalent than in hearts with only healed myocardial infarction or hearts lacking an acute or a healed myocardial infarction (89%, 46%, and 50%, respectively; P < .005). Hearts without acute or healed myocardial infarction and without active lesions were similar to hearts with active lesions with respect to heart weight and severity of epicardial coronary disease. CONCLUSIONS: Acute changes in coronary plaque morphology (thrombus, plaque disruption, or both) were found in 57% of cases of sudden coronary death. In hearts with myocardial scars and no acute infarction, active coronary lesions were identified in 46% of cases. Neither myocardial infarction (acute or healed) nor an active coronary lesion was present in 19% of hearts.     

QT dispersion may be a useful adjunct for detection of myocardial infarction in the chest pain center

BACKGROUND: QT dispersion has been proposed as a noninvasive measurement of the degree of inhomogeneity in myocardial repolarization. Increased QT dispersion has been reported after myocardial infarction. We hypothesized that increased QT dispersion may be a useful adjunct for risk stratification in patients being evaluated in a chest pain center. METHODS AND RESULTS: Patients were admitted to the chest pain center for evaluation of chest pain. Exclusion criteria included (1) systolic blood pressure <90 mm Hg, (2) ischemia or infarction on the initial electrocardiograph (ECG), (3) elevated creatine kinase or MB fraction, and (4) chest pain associated with cocaine use. Serial creatine kinase and MB levels and ECGs were obtained at 0, 6, and 9 hours. Patients were monitored for (1) creatine kinase and MB rise, (2) ECG changes for infarction, (3) ST-segment changes, and (4) rest angina. A negative evaluation at the chest pain center led to an exercise stress test. Patients with a positive exercise stress test were admitted for further evaluation and patients with a negative exercise stress test result were discharged home. Patients were divided into 3 groups. Group 1 consisted of patients who were found to have an acute myocardial infarction (AMI), group 2 consisted of patients with prior history of coronary artery disease but no evidence of AMI, and group 3 consisted of patients without prior coronary artery disease or AMI. QT dispersion was measured on the initial ECG in all patients. A total of 586 patients were evaluated. Group 1 consisted of 13 patients with mean QT dispersion of 44.6+/-18.5 ms, group 2 consisted of 267 patients with a mean QT dispersion of 10.0+/-13.8 ms, and group 3 consisted of 303 patients with a mean QT dispersion of 10.5+/-10.0 ms. Analysis of variance showed a significantly higher QT dispersion in patients who had AMI compared with other patients with chest pain (P< .001). CONCLUSIONS: QT dispersion can be a useful diagnostic adjunct for detection of AMI in patients with chest pain with a normal ECG and normal cardiac enzymes.     

Prognostic influence of increased fibrinogen and C-reactive protein levels in unstable coronary artery disease. FRISC Study Group. Fragmin during Instability in Coronary Artery Disease

BACKGROUND: The prognostic influences of fibrinogen and C-reactive protein levels and their relations to myocardial damage in unstable coronary artery syndromes have not been well described. METHODS AND RESULTS: Fibrinogen and C-reactive protein were determined at inclusion and related to outcome after 5 months in 965 patients with unstable angina or non-Q-wave myocardial infarction randomized to 5 weeks with low-molecular-weight heparin or placebo. The probabilities of death were 1.6%, 4.6%, and 6.9% (P=.005) and the probabilities of death and/or myocardial infarction were 9.3%, 14.2%, and 19.1% (P=.002), respectively, in patients stratified by tertiles of fibrinogen (< 3.38, 3.38 to 3.99, and > or = 4.0 g/L). The probabilities of death were 2.2%, 3.6%, and 7.5% (P=.003) after stratification of patient data by tertiles of C-reactive protein level (< 2, 2 to 10, and > 10 mg/L). In logistic multiple regression analysis, increased fibrinogen levels were independently associated with the incidence of death and/or myocardial infarction (P=.013), and elevated C-reactive protein level was associated with the incidence of death (P=.012). The increased relative risk of subsequent death or myocardial infarction in individuals with an elevated fibrinogen level was consistent in most subgroups evaluated; although significantly so only in patients with signs of myocardial damage. CONCLUSIONS: Increased levels of both fibrinogen and C-reactive protein are associated with a worse outcome in patients with unstable coronary artery disease. The increased risk associated with elevated fibrinogen levels is independent of, and additive to, the prognostic influence of myocardial damage.     

Noninvasive myocardial imaging with potassium-43 and rubidium-81 in patients with left bundle branch block

Noninvasive myocardial imaging with potassium-43 and rubidium-81 has been used successfully to identify areas of infarction and exercise-induced ischemia as regions of decreased radioactivity. The image defects observed are believed to be due to a decreased radionuclide uptake in regions of myocardial scar or to heterogeneous myocardial accumulation of tracer as a result of regional ischemia. Of 27 patients with left bundle branch block studied with noninvasive imaging at rest and during exercise, 25 manifested at rest reduced radioactivity in the region of the interventricular septum. This pattern is similar to that seen in patients with anteroseptal myocardial infarction. Sixteen of the 27 patients underwent diagnostic coronary arteriography and left ventriculography. Only five of these patients had evidence of either previous infarction or significant obstructive coronary artery disease as assessed with clinical or angiographic criteria, or both. Although the image defect was routinely demonstrated at rest in patients with left bundle branch block, this defect was generally normalized or less distinct with exercise in patients with no anatomic heart disease. In contrast, a larger, more distinct or new image defect with exercise correctly identified the presence of significant obstructive coronary artery disease in patients with left bundle branch block. In the clinical application of noninvasive myocardial imaging, these image defects observed at rest can lead to the false pasitive radionuclide interpretation of anteroseptal myocardial infarction.     

Hostility, social support, and coronary heart disease in the National Heart, Lung, and Blood Institute Family Heart Study

This cross-sectional study investigated the association of hostility and social support to coronary heart disease (CHD) in 2 groups of men and women: those with a familial predisposition for CHD (high-risk sample) and a randomly selected group. The hypothesis was that hostility and low social support would be associated with CHD, and would have a greater effect in the high-risk group. The random sample contained 2,447 individuals (47.1% male) from 576 families, and the high-risk sample consisted of 2,300 people (45.5% male) from 542 families. Odds ratios (OR) and their 95% confidence intervals were calculated using generalized estimating equations (GEE) for logistic regression. Family was specified as the clustering variable, and robust SEEs were obtained to account for dependence of the data within families. After controlling for age, education, body mass index, exercise, smoking history, drinking history, and drinking >5 drinks a day, hostility was associated with a history of coronary bypass surgery or coronary angioplasty in high-risk men (OR 1.21) and a history of myocardial infarction in high-risk women (OR 1.39). High-risk women with high social support had reduced odds of a previous myocardial infarction (OR 0.76), whereas women with high network adequacy in the random sample had reduced risk of myocardial infarction (OR 0.41) and angina (OR 0.49). A ratio of high hostility to low social support was associated with past myocardial infarction in high-risk women (OR 2.47) and a history of angina (OR 2.02) in the random sample men. These results suggest that high hostility and low social support are associated with some manifestations of CHD after controlling for adverse health behaviors.