Management of the older patient with acute myocardial infarction: difference in clinical presentations between older and younger patients

The majority of persons sustaining acute myocardial infarction are older, and in these older persons morbidity and mortality are high. Clinical presentations and characteristics are significantly different between older and younger infarction patients. Older infarction patients are more likely to be female and to have a history of heart failure, but they are less likely to have a family history of myocardial infarction, elevated cholesterol, or to smoke. Older patients will frequently have unrecognized or silent myocardial infarctions or, when present, symptoms will be atypical. Instead of chest pain, older patients may have shortness of breath or neurological symptoms, such as confusion. Also, older infarction patients will delay longer in seeking medical assistance after onset of symptoms, and often will not demonstrate ST elevation or Q waves on their electrocardiograms. Not infrequently, older infarction patients will demonstrate major complications such as heart failure or right ventricular infarction on hospital admission, and their presenting complaints will reflect these complications. Because of these atypical presentations and the wide variability of symptoms, physicians must be highly suspicious of the presence of an acute myocardial infarction in older patients who have an unexplained acute change in their physical condition.     

Incidence and prevalence of recognised and unrecognised myocardial infarction in women. The Reykjavik Study

AIMS: The incidence and prevalence of recognised and unrecognised myocardial infarction were determined in the Icelandic cohort study of 13,000 women (the Reykjavik Study), followed for up to 29 years (mean 15 years). METHODS AND RESULTS: Women attending the Reykjavik Study, born between 1908 and 1935, were examined in five stages from 1968 to 1991. A health survey included history and ECG manifestations of coronary heart disease. Data retrieved from hospitals, autopsy records and death certificates identified 596 fatal and non-fatal myocardial infarctions to the end of 1992 (61 prior to examination, 320 non-fatal and 215 fatal). The incidence of recognised myocardial infarction ranged from 22 cases/100,000/year at 35-39 years to 1800 cases/100,000/year at 75-79 years. The incidence of unrecognised myocardial infarction ranged from 18 cases/100,000/year at 35 years to 219 cases/100,000/year at 75 years. Thirty-three percent of non-fatal myocardial infarctions were unrecognised. More occurred in the younger age groups (40%) than in the older (27%). The prevalence of recognised myocardial infarction was influenced by age and calendar year. In 1990, it was 1.3/1,000 at 35 years and 60/1000 at 75 years. Prevalence showed a time trend, tripling in all age groups from 1968-1992. Fore unrecognised myocardial infarction, prevalence rose from 0.9/1000 at 35 years to 19.2/1000 at 75 years, although there was no evident time trend. CONCLUSION: Myocardial infarction in women is very age-dependent with both incidence and prevalence increasing continuously and steeply with age. There was a significant trend for an increase in prevalence of recognised myocardial infarction from 1968 to 1992. The proportion of unrecognised non-fatal infarctions ranged from 27% in the oldest age group to 40% in the youngest. On average, this form of coronary heart disease is as common as in men.     

Improved long-term prognosis after myocardial infarction 1984-1991

AIMS: We set out to examine whether long term prognosis in terms of 2-year mortality after myocardial infarction has improved after the introduction of intravenous beta-blockers, nitroglycerin infusion, aspirin and thrombolytics, in an unselected population of patients hospitalized with a myocardial infarction. METHODS AND RESULTS: We investigated retrospectively 3791 acute myocardial infarctions in 3187 G?teborg women and men (1039 women and 2148 men), who were consecutively admitted to the coronary care unit at the Ostra hospital during 1984-1991. Throughout this period, data were entered continuously into the coronary care unit database. Mortality data were collected through the Swedish cause-specific mortality register. The primary end-point was mortality within 2 years after the onset of the index infarction. Two-year mortality decreased from 36% in 1984 to 25% in 1991. In a Cox regression model (including myocardial infarctions up to 1993) year of hospitalization, age, diabetes mellitus, sex, prior myocardial infarction and indeterminable infarct location all had a significant impact on survival after myocardial infarct. Thrombolytic therapy and hypertension had no prognostic significance. CONCLUSION: Against a background of radical changes in the treatment of acute myocardial infarction during 1984-1991 we have seen decreasing in-hospital mortality as well as a substantial decrease in 2-year mortality.     

Small animal model for myocardial infarction

Myocardial infarctions were produced in rats by electro-cauterization of the left anterior descending artery, and the extent of myocardial damage was measured by serial serum levels of creatine phosphokinase activity utilizing spectrophotometric analysis. All animals were also evaluated for myocardial damage by electrocardiographic wave alterations. A correlation between myocardial infarct size and serum creatine phosphokinase was demonstrated. Significant arrhythmias and death occurred only in experimental groups where myocardial infarction had been produced. This small animal model offers a quick, inexpensive, and simple method for screening therapeutic agents that alter infarct size.     

Growth hormone stimulates the tyrosine kinase activity of JAK2 and induces tyrosine phosphorylation of insulin receptor substrates and Shc in rat tissues

Each year, acute myocardial infarctions (AMI) account for more than half a million deaths in the United States. Complicating treatment of AMI is the difficulty in accurately diagnosing the event, for patients have nondiagnostic electrocardiograms (ECG) more than 50% of the time. In this population, cardiac markers are essential to confirm the diagnosis. The new bedside cardiac markers, which use eight drops of whole blood and require 15 minutes to be read negative, make it possible to shorten time needed to diagnose AMI. One hundred twenty-seven consecutive patients presented to the emergency department complaining of atypical chest pain. All had ECGs that were nondiagnostic for myocardial infarction. Serial cardiac markers were performed: myoglobin, troponin I, rapid myoglobin, and rapid troponin I. One hundred eighteen patients with negative serial cardiac markers had exercise treadmill tests in the emergency department. Nine patients with positive serial cardiac markers received emergent primary angioplasty. Six of the nine patients were treated based on the positive results of the rapid bedside cardiac markers. A 100% correlation existed between the quantitative serum results and the rapid bedside markers. With the availability of rapid bedside assays, dependency on the laboratory can be minimized, since quantitative cardiac markers require at least 1 hour of turnaround time. Rapidly and correctly diagnosing AMIs in patients with ECGs nondiagnostic for AMI has always been a dilemma. Rapid bedside assays enable the physician to accurately diagnose myocardial infarction and safely decrease the time in evaluating chest pain, thus maximizing the benefits of early reperfusion.     

Morphologic investigations on experimental coronary thromboses in pigs (author''s transl)

By means of electric induction without opening the chest in 23 dogs coronary thromboses were produced with the aid of a standardized method based on a test model of Salazar (1961). The morphological results are reported. 13 of the dogs showed coronary thromboses. At the same time in 12 animals a myocardial infarction could be registered. Altogether, we observed 17 myocardial infarctions. The electric field led to differently severe lesions in the walls of the coronary arteries. The significance of this test model is discussed.     

Controversy about using calcium antagonists for treatment of coronary disease and hypertension

Calcium antagonists are widely used in therapy of hypertension and angina pectoris. Their advantage is good efficacy, relatively few and not dangerous side effects and first of all lack of bad metabolic effects (hypokalemia, hyperuricemia, hyperinsulinemia and hyperlipoproteinemia). In contrast to beta-blockers and diuretics, which decline mortality from myocardial infarctions and strokes there are not similar information concerning calcium antagonists. Two meta-analysis from 1995 unexpectedly suggest, that some preparations of calcium antagonists increase mortality from myocardial infarctions and strokes. In our paper we discuss possible pathogenetic (harmful) mechanisms, pay attention to each class of calcium antagonists and time of action of the particular drugs. Short acting nifedipine formulation should be withdrawn from chronic hypertension and angina pectoris therapy. Ongoing multicenter trials in several European countries and in USA will decide the usefulness of other calcium antagonists preparations.     

Detailed examination of vascular lesions triggered by an inhibitor of endothelium-derived relaxing factor

BACKGROUND: Inhibition of an endothelium-derived relaxing factor (EDRF) may contribute to the pathogenesis of thrombotic arterial occlusions. EXPERIMENTAL DESIGN: We measured the blood pressure and urinary excretion of protein, sodium, and potassium and histologically examined the brains, hearts, and kidneys in normotensive Wistar Kyoto rats (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP) fed on a diet containing: (a) EDRF inhibitor (L-N-nitroarginine:L-NNA); (b) L-arginine, which reverses the effect of L-NNA; or (c) both L-NNA and L-arginine for 1 to 8 weeks. In addition, we examined L-NNA-treated SHRSP, the blood pressures of which were lowered using hydralazine. Furthermore, we produced and examined Goldblatt's renal hypertensive rats, which are of a different type from those resulting from the L-NNA treatment. RESULTS: Both WKY and SHRSP rats fed on a diet containing L-NNA suffered from hypertension and cerebral infarctions in a dose-dependent manner. Cerebral infarctions occurred whether or not SHRSP rats were treated with an antihypertensive agent when they were fed a high dosage of L-NNA. In contrast, SHRSP rats, treated simultaneously with both L-NNA and L-arginine, suffered few cerebral infarctions, although they were severely hypertensive. In addition, there were no cerebral infarctions in Goldblatt's renal hypertensive rats, although they suffered from advanced hypertension. CONCLUSIONS: The data indicate that the inhibition of EDRF injures the vessel walls and encourages platelet adhesion to the damaged areas. The adhering platelets narrow the lumen with resultant thrombotic arterial occlusions. Pathophysiologic conditions that decrease EDRF synthesis appear to play an important role in cerebral, renal, and myocardial infarctions.     

Perfusion scintigraphy of the myocardium in cardiological diagnosis. Coronary diseases, primary myocardial diseases and rheumatic heart valve diseases

In 123 patients perfusion scintigrams were compared with the data of clinical investigation, right and left heart catheterisation and coronary arteriography. The intracoronary application of radioactive labelled human-albumin-microspheres and human-microaggregates were without any complications. The patients suffered from coronary heart diseases, primary myocardial diseases and rheumatic valvula heart diseases. There was a good correlation between the myocardial perfusion defect and the degree of coronary artery stenoses. Furthermore an excellent correlation was found between perfusion defects and levocardiographic findings: left ventricular aneurysms, akinetic or hypokinetic areas and the ejection fraction of the left ventricle. All myocardial infarctions were detected by a perfusion defect in the scintigrams. In 16 cardiacsurgery-patients large myocardial perfusion defects were found to be myocardial scars. In primary myocardial diseases perfusion scintigraphy is an effective method of detecting pathological myocardial patterns. The degree of perfusion defects correlates excellently with the levocardiographic findings. It seems that in rheumatic valvular diseases perfusion-scintigraphy is a method to discover rheumatic myocardial abnormalities--probably scar tissue. In comparison with thallium scintigrams it was shown that extensive myocardial failures (aneurysms) can be represented by both nuclear medical procedures but that perfusion scintigraphy is more sensitive and correlates more closely to the levocardiogram findings.     

Disposition of presumed coronary patients from an emergency room. A follow-up study

All patients with presumed coronary problems seen at the Chaim Sheba Medical Center during a one-year period were followed up. The fate of those who were not hospitalized and the factors contributing to the two types of erroneous decisions, ie, refusing hospitalization to those needing it and unnecessary hospitalization of others, were evaluated. Approximately 50% of the patients were not admitted. Myocardial infarctions were later diagnosed in 6% of these patients. Another 8% were eventually categorized as other cardiac emergencies. Ten percent of all patients subsequently diagnosed as having myocardial infarctions were not admitted. On the other hand, 56% of the patients whose cases were later not considered to have been emergencies were hospitalized unnecessarily. Previous hospitalization for cardiac disease played a major role in making an error of both types. Other factors influencing the physician's decision regarding the patients' disposition included their age, sex, ethnic origin, and the findings from the emergency room electrocardiogram.     

The effects of normal as compared with low hematocrit values in patients with cardiac disease who are receiving hemodialysis and epoetin

BACKGROUND: In patients with end-stage renal disease, anemia develops as a result of erythropoietin deficiency, and recombinant human erythropoietin (epoetin) is prescribed to correct the anemia partially. We examined the risks and benefits of normalizing the hematocrit in patients with cardiac disease who were undergoing hemodialysis. METHODS: We studied 1233 patients with clinical evidence of congestive heart failure or ischemic heart disease who were undergoing hemodialysis: 618 patients were assigned to receive increasing doses of epoetin to achieve and maintain a hematocrit of 42 percent, and 615 were assigned to receive doses of epoetin sufficient to maintain a hematocrit of 30 percent throughout the study. The median duration of treatment was 14 months. The primary end point was the length of time to death or a first nonfatal myocardial infarction. RESULTS: After 29 months, there were 183 deaths and 19 first nonfatal myocardial infarctions among the patients in the normal-hematocrit group and 150 deaths and 14 nonfatal myocardial infarctions among those in the low-hematocrit group (risk ratio for the normal-hematocrit group as compared with the low-hematocrit group, 1.3; 95 percent confidence interval, 0.9 to 1.9). Although the difference in event-free survival between the two groups did not reach the prespecified statistical stopping boundary, the study was halted. The causes of death in the two groups were similar. The mortality rates decreased with increasing hematocrit values in both groups. The patients in the normal-hematocrit group had a decline in the adequacy of dialysis and received intravenous iron dextran more often than those in the low-hematocrit group. CONCLUSIONS: In patients with clinically evident congestive heart failure or ischemic heart disease who are receiving hemodialysis, administration of epoetin to raise their hematocrit to 42 percent is not recommended.     

What is 'minimally invasive' coronary bypass surgery? Experience with a variety of surgical revascularization procedures for single-vessel disease

BACKGROUND: Although the use of small incisions is theoretically appealing, it has been argued that the true advantage of minimally invasive approaches to myocardial revascularization lies in the avoidance of cardiopulmonary bypass. METHODS: Of 25 patients referred for surgical revascularization of single-vessel coronary disease, 20 elected to undergo a minimally invasive coronary artery bypass grafting (MICABG) procedure, while 5 opted to have conventional surgery with cardiopulmonary bypass (CPB). Patients having MICABG underwent single-vessel revascularization without CPB, via limited anterior thoracotomy, hemisternotomy, or median sternotomy. Intraoperatively, hemodynamics, anastomotic time, and total operative time were recorded. Postoperatively, length of hospital stay, incidence of myocardial infarction, indexes of end-organ function, and morbidity rates were recorded. In addition, patient questionnaires were used to assess subjective end points such as postoperative pain, wound drainage, and quality of life. RESULTS: Fifteen of 20 patients undergoing MICABG underwent revascularization without CPB, while 4 were converted to standard coronary artery bypass grafting with CPB due to technical reasons and 1 for intraoperative ventricular fibrillation. Patients undergoing MICABG had no perioperative myocardial infarctions, while those having CPB had two infarctions (20%). Furthermore, there were no differences in length of stay or postoperative morbidity among the various approaches, while the MICABG procedures, especially via median sternotomy, were associated with shorter operative times. CONCLUSIONS: The advantage of MICABG lies mainly in the avoidance of CPB. Thus, we advocate that surgeons initially utilize the median sternotomy and limited skin incision for MICABG to assure adequate exposure, technical precision, and patient safety. After a reasonable level of technical proficiency and experience are attained, the limited anterior thoracotomy approach can be used.     

Diagnosis of right ventricular infarction by overlap images of simultaneous dual emission computed tomography using technetium-99m pyrophosphate and thallium-201

The validity of dual energy single-photon emission computed tomography (SPECT) with technetium-99m pyrophosphate (Tc-99m PPi) and thallium-201 for the diagnosis of right ventricular (RV) infarction, and the clinical features of RV infarction, were investigated in 190 patients with acute myocardial infarction. Diagnosis of RV infarction was performed by Tc-99m PPi accumulation in the RV myocardium on thallium-201 and Tc-99m PPi over-lay images at the dual SPECT with simultaneous imaging taken 2 to 9 days after the onset of myocardial infarction. Thirty RV infarctions were found among the 190 patients with left ventricular infarction (15.8%): 29 (97%) in association with the inferior and 1 (3%) with the lateral infarction. Tc-99m PPi accumulation was mostly observed in the posterior wall of the right ventricle. A total occlusion or a severe stenosis of the right coronary artery was demonstrated angiographically in 92% of the patients with RV infarction. The prevalence of RV infarctions was significantly lower in patients who achieved successful early reperfusion than in those who did not (26.7 vs 68.4%, respectively, p < 0.01). However, a successful early reperfusion therapy could not significantly decrease the rate of RV involvement in patients without significant collateral flow (p < 0.01). Thus, dual isotope SPECT with Tc-99m PPi and thallium-201 can be used as a reliable method for the diagnosis of RV infarction.     

Selective coronary arteriography. Risk in a community hospital

Over a 33-month period, selective coronary arteriography was performed in 627 consecutive patients in a 385-bed, non-university-affiliated community hospital. Mortality was 0.16% (one death); there was also one nonfatal myocardial infarction. No deaths or myocardial infarctions occurred in the last 369 consecutive patients in this series when routine systemic heparinization was introduced. Substantially greater risk of mortality (2.6%) and nonfatal myocardial infarction (2.6%) was encountered in an earlier series of 78 consecutive patients for whom a different protocol was used. It included extensive exercise hemodynamic studies with the use of percutaneous arterial angiographic catheters, without systemic heparinization. This indicates that coronary arteriography can be carried out with acceptable risk in a community hospital. Protocols should be designed to minimize the time that catheters are in the arterial system. Systemic heparinization may reduce the risk of procedure-related death and myocardial infarction.     

Mismatch between myocardial accumulation of 123I-MIBG and 99mTc-MIBI and late ventricular potentials in patients after myocardial infarction: association with the development of ventricular arrhythmias

BACKGROUND: Late ventricular potentials are widely used to predict life-threatening arrhythmias, although the predictive value is low. To improve prediction, we correlated the incidence of ventricular arrhythmias with mismatches in myocardial 99mTc-methoxyisobutylisonitrile (MIBI)/(123)I-metaiodobenzylguanidine (MIBG) accumulation and late ventricular potentials (LP). METHODS AND RESULTS: Fifty patients with old myocardial infarctions were divided into an LP-positive group (n = 19) and an LP-negative group (n = 31). On bull's-eye single photon emission computed tomographic MIBI and MIBG images, the heart was divided into 9 segments to evaluate the accumulation of the 2 nuclides. There was no difference in total defect score (TDS) for MIBI between the LP-positive and LP-negative groups. However, TDS for MIBG and differences TDS between MIBI and MIBG (ATDS) were significantly greater in the LP-positive group. CONCLUSIONS: The incidence of severe ventricular arrhythmias was greater among patients with an increased ATDS in the LP-positive group. Thus the combination of these two methods may improve the prediction of ventricular arrhythmias after myocardial infarction.     

Acute myocardial infarct and left ventricular dysfunction. Morphologic bases, clinical aspects and pharmacologic prevention

The morphological bases which condition left ventricular disfunction after acute myocardial infarction as well as the concepts of expansion and remodelling of the myocardium are reviewed. The clinical aspects indicating ventricular disfunction are presented and several pharmacological effects which have been proposed for the prevention of this situation. Particular emphasis is given to the role of angiotensin-converting enzyme inhibitors in the prevention of left ventricular disfunction after acute myocardial infarctions, based on the most recent clinical trials.     

Renal failure after two myocardial infarctions

A 60-year-old man was admitted to the hospital for elective cardiac catheterization. He had had two myocardial infarctions (MI) one and two months earlier. After the second MI, he had been treated with tissue plasminogen activator and heparin. Since then, his blood urea nitrogen concentration had increased from 20 to 63 mg/dL and his blood creatinine concentration from 1.2 to 9.2 mg/dL.     

Dobutamine-atropine stress echocardiography in elderly patients unable to perform an exercise test. Hemodynamic characteristics, safety, and prognostic value

OBJECTIVE: To establish the hemodynamic effects, safety, and prognostic value of dobutamine-atropine stress echocardiography in patients 70 years of age or older. DESIGN AND SETTING: Observational study at a university hospital. PATIENTS: One hundred seventy-nine patients (mean age, 75 years; range, 70 to 90 years) referred for chest pain (n = 73) or preoperative risk assessment for major vascular noncardiac surgery (n = 106). MEASUREMENTS: All patients underwent clinical evaluation and dobutamine-atropine stress test. RESULTS: One hundred seventy-nine stress tests were performed. Test end points were the target heart rate (85% of theoretical maximum heart rate), reached in 165 tests (92%); inadequate echo images, two tests (1%); and side effects, 12 tests (7%). Side effects that caused a premature end of the test were severe chest pain (n = 5 [2.8%]), electrocardiographic changes (n = 1 [0.6%]), hypotension (n = 2 [1.1%]), chills (n = 2 [1.1%]), and cardiac arrhythmias (paroxysmal atrial fibrillation) (n = 2 [1.1%]). New wall motion abnormalities as a marker of myocardial ischemia occurred in 50 tests (28%). No death or myocardial infarction occurred during the test. Perioperative events occurred in 12 patients (four cardiac deaths, three myocardial infarctions, and five episodes of unstable angina). During 16 +/- 6 months (mean +/- SD) of follow-up of 166 patients, 22 cardiac events occurred (eight cardiac deaths, four myocardial infarctions, and 10 episodes of unstable angina pectoris). By multivariate regression analysis, only perioperative cardiac events (odds ratio, 51; 95% confidence interval, 5.8 to 454) and late cardiac events (odds ratio, 5.2; 95% confidence interval, 2.0 to 14) were correlated with new wall motion abnormalities during stress. CONCLUSION: Dobutamine-atropine stress echocardiography is a feasible and safe test for assessing elderly patients with suspected and/or proven coronary artery disease, providing useful prognostic information for perioperative and late cardiac risk with relatively few side effects.     

Troponin T in patients with low grade or atypical angina. Identification of a high risk group for short- and long-term cardiovascular events

AIMS: Cardiac troponin T is an established marker of cardiovascular risk in patients with severe angina pectoris. Data are scarce on patients admitted to a coronary care unit with low grade or atypical angina pectoris to rule out myocardial infarction. METHODS AND RESULTS: We investigated 106 patients (57.4 SD 11.6 years) with low grade (Braunwald class I) or atypical symptoms out of 702 patients admitted to the coronary care unit with suspected acute myocardial infarction. Serum concentrations of troponin T were measured at admission and 4 h later. In hospital cardiovascular events including acute myocardial infarction, life threatening cardiac arrhythmias, congestive heart failure, and death were recorded. Patients were additionally observed after 3 and 6 months post-discharge regarding acute myocardial infarction, unstable angina, rehospitalization for cardiac causes and death. The patients were divided into a troponin T positive (> or =0.2 microg x 1(-1) at admission or 4 h later; n=11) and a troponin T negative group. The mean value of troponin T 4 h after admission in the positive group was 0.58 microg x 1(-1). Of the troponin T positive patients, 0.82 (0.95 CI: 0.48-0.98) had a cardiovascular event during their stay in hospital vs 0.41 (0.95 CI: 0.31-0.52) of troponin T negative patients (P<0.05). In the troponin T positive group 0.64 (0.95 CI: 0.31-0.89) developed myocardial infarction in hospital vs 0.07 (0.95 CI: 0.03-0.15) in the troponin T negative group (P<0.001). Troponin T predicts outcome after 3 and 6 months significantly (P<0.05). CONCLUSION: Troponin T identifies patients with low grade or atypical angina at risk of severe short- and long-term cardiovascular events. Therefore, troponin T adds substantial information in patients with ruled out acute myocardial infarction. Troponin T positive patients have to be observed carefully regardless of their symptom intensity and may have to receive early cardiac catheterization; troponin T negative patients could be released safely from the coronary care unit early.     

Results of long-term administration of anticoagulants in patients with myocardial infarction and coronary heart disease without infarction

Long-term treatment with anticoagulants (Sintrom, Suncumar) was applied in 300 cases of myocardial infarction and 106 cases of coronary heart disease without infarction aged 31 to 70 years over periods ranging from one to six years. The control group comprised 347 patients with myocardial infarction and 195 patients with coronary heart disease without infarction in the same age range who were not treated with Syncumar because of contraindications. Treatment with Syncumar was started on the first day at hospital and was continued after discharge from the hospital on an outpatient basis. The level of prothrombin was kept within the range of 35-45%. In the Syncumar treated group the mortality in patients with myocardial infarction was 8.0% and in the control group it was 20.5%. In the Syncumar treated group the incidence of repeated infarctions was 12.7% and in the controls it was 33.1%. On the other hand, no effects of Syncumar on the mortality of patients with chronic coronary heart disease without infarction was observed.