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PubMed1993

[Fatty acid composition of plasma lipids in hyperlipidemia associated with ischemic heart disease].

The authors compared plasma lipid and lipoprotein values and the fatty acid composition in plasma lipids of a group of 38 men with primary hyperlipoproteinaemia (HLP) type II B and IV with a history of myocardial infarction (IM) and in a control group of 63 men with the same type of HLP without a history of ischaemic heart disease (IHD). Hyperlipidaemic subjects after IM differed from controls by the apolipoprotein (apo) B concentration in LDL lipoproteins and by the composition of fatty acids in plasma phosphatidylcholine (PC) and triglycerides (TG). In the discriminating function which makes it possible in the given group of patients to classify correctly hyperlipidaemic subjects after IM and without detectable IHD the independent variables are apo-B concentration in LDL, apo-A-I in plasma, eicosapentaenoic acid in TG, gamma-linolenic acid in cholesterol esters and stearic and oleic acid in PC. These findings confirm the practical value of assessment of apolipoproteins for detection of hyperlipidaemic subjects with a specially high risk of IHD and indicate also the role of essential FA in the pathogenesis of IM.

Fatty Acids↗
PubMed2004

Reteplase monotherapy and reteplase/abciximab combination therapy in peripheral arterial occlusive disease: results from the RELAX trial.

PURPOSE: The safety and efficacy of increasing doses of intraarterial reteplase monotherapy and reteplase/abciximab combination therapy were examined in patients with acute peripheral arterial occlusive disease (PAOD). The primary endpoint of this analysis was major bleeding as defined by the Thrombolysis in Myocardial Infarction (TIMI) investigators. MATERIALS AND METHODS: The RELAX trial was a prospective, dose-escalating safety trial of reteplase monotherapy (0.1, 0.2, 0.5, or 1.0 U/h) and reteplase/abciximab combination therapy (0.25-mg/kg bolus and 0.125 micro g/kg/min abciximab in addition to each reteplase regimen) for patients with acute or subacute clinical deterioration of PAOD. Reteplase was administered intraarterially to 74 patients; 38 patients were also administered intravenous abciximab for the duration of reteplase infusion. Protocol-specified angiograms were obtained at 6 and 20 hours or for clinical need. Each angiogram was assessed for volume of thrombus dissolved and for arterial patency. The primary safety endpoint (TIMI major bleeding) was assessed at discharge and at day 7. Clinical endpoints were assessed at discharge and at days 30 and 90. RESULTS: Major bleeding occurred with similar frequency in patients treated with and without abciximab (15% of the pooled patients receiving reteplase monotherapy and 20% of patients receiving reteplase/abciximab combination therapy). There were no intracranial hemorrhagic events in the 74 patients. Reteplase doses of at least 0.2 U/hour were effective at dissolving thrombus and restoring patency. There was no clear dose-response relationship for reteplase. However, the addition of abciximab reduced the occurrence of distal embolic events requiring intervention (5% vs. 31%; P =.014). CONCLUSIONS: Over the range of reteplase doses studied for peripheral arterial thrombolysis, there were no significant differences in safety or efficacy. However, the addition of intravenous abciximab to reteplase was associated with a decreased rate of distal embolic events without a significant increase in the risk of hemorrhagic complications. Further investigation is needed to define the role of abciximab in catheter-directed thrombolysis with reteplase for PAOD.

Abciximab↗
PubMed2001

Characteristics of 15,314 hypertensive patients at high coronary risk. The VALUE trial. The Valsartan Antihypertensive Long-term Use Evaluation.

Valsartan is an orally active, selective antagonist of the angiotensin II-1 (AT1) receptor developed for the treatment of hypertension. The Valsartan Antihypertensive Long-term Use Evaluation (VALUE) Trial of Cardiovascular Events in Hypertension is a double-blind, randomized prospective, parallel group study designed to compare the effects of valsartan with those of the calcium-antagonist amlodipine on the reduction of cardiac morbidity and mortality. Patients with essential hypertension, aged 50 years and older, and at particularly high risk of coronary events were enrolled. 18,119 patients were screened and 15,314 patients in 31 countries were randomized mainly between January 1998 and December 1999. These hypertensives had a mean blood pressure of 154.7/87.5 mmHg at the time of their randomization to blinded medication. The population comprises both genders (men 57.6%), Caucasians (89.1%), mean age 67.2 years, mean body mass index 28.6 kg/m2, coronary heart disease (45.8%), high cholesterol (33.0%), type 2 diabetes mellitus (31.7%) and smokers (24.0%). More than 92% of the randomized participants had been treated for high blood pressure for at least 6 months when screened for the study. The randomized population is now being treated (goal blood pressure < 140/90 mmHg) in adherence with the protocol until at least 1450 patients experience primary cardiac endpoint defined as clinically evident or aborted myocardial infarction, hospitalization for heart failure or death caused by coronary heart disease.

Aged↗
PubMed1998

Natural history of myocardial infarction and angina pectoris in a general population sample of middle-aged men: a 16-year follow-up of the Primary Prevention Study, Göteborg, Sweden.

OBJECTIVES: Although many studies have described prognosis in patients with coronary heart disease (CHD), few have compared outcome in men with clinical evidence of CHD with healthy men from the general population over an extended follow-up. This study aimed to compare long-term prognosis in men with a history of myocardial infarction (MI) and in men with angina pectoris (AP) without MI, with men without clinical signs of CHD. DESIGN: Longitudinal general population study. SETTING: City of Göteborg, Sweden. SUBJECTS: From a general population sample, 195 men who had survived an MI for 0-19 years (median 3 years) and 314 men with AP but no MI (uncomplicated AP) at baseline in 1974-77 were identified and compared with 6591 men without clinical coronary disease. All were aged 51-59 years. Incident non-fatal and fatal cases occurring until the beginning of 1983 were also followed (n = 317). MAIN OUTCOME MEASURES: Death from CHD, from other causes and from all causes during a follow-up of at least 16 years. RESULTS: Overall survival was 72% amongst men without coronary disease, 53% amongst men with uncomplicated AP and 34% amongst men with past MI at baseline. In survivors of MI the risk-factor-adjusted relative risk (RR) of coronary death during follow-up was 6.67 (95% confidence interval (CI) 5.29-8.39), of dying from non-cardiovascular causes 1.35 (0.96-1.91), and of dying from any cause 3.20 (2.67-3.83). During the first 4 years after the baseline examination, the adjusted RR of CHD death was 15.96 (10. 29-24.74), and of dying from any cause 5.22 (3.68-7.41). During the last 4 years of follow-up, relative risk was still 5.87 (3.44-10.01) for CHD death and 2.93 (2.05-4.18) for death from any cause. In men with uncomplicated AP, the adjusted relative risk of CHD death during the first 4 years was 4.05 (2.27-7.22) and 3.23 (2.10-4.96) during the last 4-year period. After the first year, the incident MI cases had the same average annual mortality (about 5%) as the prevalent cases. CONCLUSIONS: In survivors of MI, mortality risk remained high even after an extended follow-up. Men with angina had a better prognosis, but still a compromised survival compared with the general population.

Angina Pectoris↗
PubMed2003

[Long-term risk of myocardial infarction after a first-ever stroke].

PURPOSE: To examine the incidence of myocardial infarction during the first three years after a first-ever stroke. MATERIAL AND METHODS: Both Kaunas community-based stroke register and ischemic heart disease register served at the primary source of data. The methods used for data collection were those applied by the World Healt Organisation (WHO) for the WHO MONICA project. During 1986 to 1994, 2531 patients aged 25 to 64 years with a first-ever stroke were registered and followed-up for three years for the information on the first-ever acute myocardial infarction or death from ischemic heart disease. Actuarial life tables were used to analyze risk of myocardial infarction. RESULTS: During the study period, 58 patients with the first-ever acute myocardial infarction that occurred among the first-ever stroke survivors were identified. Fifty-three first-ever ischemic stroke survivors (39 (73.6%) men and 14 (26.4%) women, (p=0.07)) experienced their first-ever myocardial infarction. The cumulative risk of suffering an acute myocardial infarction was 3.5% (95% confidence interval 2.6 to 4.4%) by 3 years: in male ischemic stroke survivors this risk accounted for 4.3% (95% confidence interval 3.0 to 5.6%) and in female - 2.3% (95% confidence interval 1.1 to 3.5%). The risk was the highest one early after ictus in the ischemic stroke survivors: 0.5% (95% confidence interval 0.2 to 0.8%) by 3 months (men - 0.7% (95% confidence interval 0.2 to 1.2%), women - 0.3% (95% confidence interval 0.0 to 0.7%)). CONCLUSION: The risk of myocardial infarction is the highest early after the first stroke, although due to relatively small number of cases confidence intervals were too wide to reach a statistical significance.

Actuarial Analysis↗
PubMed1986

Is relationship between serum cholesterol and risk of premature death from coronary heart disease continuous and graded? Findings in 356,222 primary screenees of the Multiple Risk Factor Intervention Trial (MRFIT).

The 356,222 men aged 35 to 57 years, who were free of a history of hospitalization for myocardial infarction, screened by the Multiple Risk Factor Intervention Trial (MRFIT) in its recruitment effort, constitute the largest cohort with standardized serum cholesterol measurements and long-term mortality follow-up. For each five-year age group, the relationship between serum cholesterol and coronary heart disease (CHD) death rate was continuous, graded, and strong. For the entire group aged 35 to 57 years at entry, the age-adjusted risks of CHD death in cholesterol quintiles 2 through 5 (182 to 202, 203 to 220, 221 to 244, and greater than or equal to 245 mg/dL [4.71 to 5.22, 5.25 to 5.69, 5.72 to 6.31, and greater than or equal to 6.34 mmol/L]) relative to the lowest quintile were 1.29, 1.73, 2.21, and 3.42. Of all CHD deaths, 46% were estimated to be excess deaths attributable to serum cholesterol levels 180 mg/dL or greater (greater than or equal to 4.65 mmol/L), with almost half the excess deaths in serum cholesterol quintiles 2 through 4. The pattern of a continuous, graded, strong relationship between serum cholesterol and six-year age-adjusted CHD death rate prevailed for nonhypertensive nonsmokers, nonhypertensive smokers, hypertensive nonsmokers, and hypertensive smokers. These data of high precision show that the relationship between serum cholesterol and CHD is not a threshold one, with increased risk confined to the two highest quintiles, but rather is a continuously graded one that powerfully affects risk for the great majority of middle-aged American men.

Adult↗
PubMed1997

The cardiac profile and proposed practice guideline for acute ischemic heart disease.

Presented with an ever-increasing array of potential tests of myocardial injury, the clinical pathologist in conjunction with physicians in primary care, cardiology, and other clinical disciplines must evolve a practical approach for each individual institution. This involves identifying the tests available for immediate (stat) or timed performance, the appropriate patients for whom testing is desired, the schedule of frequency and duration of testing, and the manner in which the test results are to be interpreted. A guideline is presented to address these issues with the purpose of stimulating local adoption of an appropriately modified version to accommodate the current state of the art. Selective choice of an early marker, creatine kinase MB by mass immunoassay, in conjunction with cardiac troponin I (cTnI), is proposed as the appropriate combination of laboratory tests that emphasizes the cardiospecificity of cTnI for the variety of applications in which the "cardiac profile" formerly has been used, including the spectrum of clinical settings in which suspected myocardial infarction must be considered. A rationale is provided with emphasis on the relative merit of the various biochemical markers in contrast with other modalities for evaluating suspected myocardial injury.

Acute Disease↗
PubMedDate not supplied

Infections, atherosclerosis, and coronary heart disease.

There is growing evidence that the immune response is involved in atherosclerosis. Studies done over the past several years have shown an association between markers of inflammation and coronary atherosclerosis with an exacerbation of the inflammatory process during acute myocardial ischemia. Overall, these data have greatly renewed interest in the infectious theory of atherosclerosis and coronary heart disease. Search of bibliographic databases (from January 1991 through December 1999) and manual scanning of both peer-reviewed publications and other documents were used to identify pertinent literature. Infections and coronary heart disease were indexed as key words. A large number of studies have reported an association of human coronary heart disease and certain persistent bacterial and viral infections. The association between Chlamydia pneumoniae and coronary heart disease appears quite significant although the sequence of infection and disease is uncertain. The association between Helicobacter pylori and coronary heart disease may be accounted for by residual confounding from classic risk factors. Preliminary findings indicate that this association could be due to a higher prevalence of more virulent Helicobacter strains. Infection with Cytomegalovirus appears to be associated with a greater risk of restenosis after angioplasty rather than primary atherosclerosis. Early trials of appropriate antibiotic therapy in subjects with recent acute myocardial infarction have been encouraging. A causal relationship between infections and coronary heart disease is still elusive. Improved studies involving prospective collection of data are required to demonstrate such an association with potential implications for public health worldwide.

Arteriosclerosis↗
PubMed2006

State of the heart: building science to improve women's cardiovascular health.

Cardiovascular disease is the No. 1 killer of women in the United States, and marked disparities in cardiovascular health exist between women and men and among groups of women. Coronary heart disease is underdiagnosed, undertreated, and under-researched in women. Women with suspected heart disease are less likely than men to receive indicated diagnostic tests and procedures; sex-based biases in treatment of myocardial infarction persist; and women continue to be underrepresented in cardiovascular research. An accumulating body of literature points to 3 major explanations: sex-based physiology, provider bias, and psychosocial influences. Women's acute and prodromal signs and symptoms of myocardial infarction have been described, yet women have difficulty recognizing and acting on these indications. Primary and secondary prevention of heart disease in women is imperative; although the science is lacking in several areas, existing evidence on diet, hormone therapy, aspirin, physical activity and obesity, and diabetes can serve as the basis for interventions. Potentially, large impacts could be made on women's morbidity and mortality if current scientific knowledge were implemented. The state of the science of women and heart disease is reviewed, with a focus on those areas with the greatest potential to address the needs of women's cardiovascular status. Key gaps in the science and remaining questions are presented as a research agenda for the coming decade.

Cardiovascular Diseases↗
PubMed2000

[Prevention of cardiovascular diseases: should the same criteria be applied in Latin America and Europe and North America?].

The prevention of cardiovascular diseases is based on the management of known cardiovascular risk factors by pharmacological means or by modifying lifestyles. A reduction in cholesterol levels is associated with a lower incidence of cardiovascular events and mortality, in both primary or secondary prevention trials. A reduction in blood pressure also leads to a decrease in acute myocardial infarction and the incidence of stroke. Regular exercise is associated with better disease free survival and the effects of smoking cessation are well known. High homocysteine levels are also associated with cardiovascular disease. However, there are no prospective clinical trials showing a beneficial effect of homocysteine reduction on cardiovascular mortality. A change in the type of dietary fat should also be beneficial, but this has not been proven in prospective clinical trials. In Chile, cardiovascular diseases are the leading cause of death among adults and the prevalence of cardiovascular risk factors, including hyperhomocysteinemia is similar to that of European or North American populations. Successful primary and secondary prevention programs to manage these risk factors have been developed in Chile. Therefore, the criteria applied in North America and Europe for the prevention of cardiovascular diseases, should be applied with slight modifications, in Latin American Countries.

Canada↗
PubMed1992

Relationship between serum total cholesterol, infarct size, and early clinical outcome following acute myocardial infarction.

Strategies designed to decrease coronary heart disease (CHD) associated morbidity and mortality have focused primarily on established risk factors, including hypercholesterolemia, systemic hypertension, and cigarette smoking. Indeed, primary and secondary intervention trials have provided evidence for cholesterol lowering as an efficient method of CHD risk reduction. To test the hypothesis that serum total cholesterol influences the clinical outcome following acute myocardial infarction, infarct size, left ventricular ejection fraction, infarct-related vessel patency, and in-hospital cardiac events were determined in 106 consecutive patients given thrombolytic therapy within 5 h of symptom onset. Cumulative 48-hour creatine kinase (CK) release, peak CK, and calculated infarct size did not differ significantly between patients with an admitting serum total cholesterol level less than 200 mg/dl (group 1) and those with a cholesterol level greater than 250 mg/dl (group 2). Total cholesterol did not correlate with either cumulative CK release, peak CK, infarct size, vessel patency, or left ventricular ejection fraction. The vessel patency correlated inversely with cumulative CK release (r = -0.27; p = 0.03) and directly with left ventricular ejection fraction (r = 0.24; p = 0.03). The incidence of in-hospital cardiac events including recurrent infarction, congestive heart failure, and death was 6.9, 13.9, and 2.6%, respectively, and did not differ significantly between patient groups. Thus, although serum total cholesterol has been shown to influence CHD incidence, morbidity, and overall mortality, the findings of our study suggest that it does not impact directly on infarct size, left ventricular function, or in-hospital clinical outcome among patients sustaining acute myocardial infarction.

Cholesterol↗
PubMed1993

A follow-up study of resected stomach cancer patients with special emphasis on the incidence of second primary cancers.

The causes of death in long-term survivors of stomach cancer after a gastrectomy have been investigated in a follow-up study of 320 such patients, with special focus on the postoperative development of a second primary cancer. The five- and 10-year overall survival rates of early stomach cancer patients were 87.5 and 75.8%, respectively, and of advanced stomach cancer patients, 44.2 and 37.5%, respectively. A multivariate analysis identified the patient's age and stage of cancer at the time of diagnosis as separate prognostic factors for overall survival. During the observation period, 15 (4.7%) patients developed a second primary cancer, so that no significantly elevated risk of developing a second primary cancer was demonstrated. During the same observation period, however, 48 (15%) of the patients died of a non-cancerous disease, 12 succumbing to an acute myocardial infarction and/or heart failure. Given these results, it is felt that continued follow-up of long-term stomach cancer survivors should be pursued to prevent or impede the development of a non-cancerous disease and/or a second primary cancer, so that the life of such former patients can be prolonged.

Adult↗
PubMed1997

Increased sarcolemmal glucose transporter abundance in myocardial ischemia.

Many clinical and laboratory studies suggest that an increase in glucose uptake and metabolism by ischemic myocardium helps protect myocardial cells from irreversible injury. We have examined whether increased sarcolemmal abundance of cardiomyocyte glucose transporters plays a role in this adaptive response. We have shown that acute myocardial ischemia in perfused rat hearts results in increased sarcolemmal abundance of the major glucose transporter, GLUT4, by causing translocation of GLUT4 molecules from an intracellular compartment to the sarcolemma. In nonischemic control hearts only 18 +/- 2.8% of GLUT4 molecules were on the sarcolemma whereas in ischemic hearts this increased to 41 +/- 9.3%. Insulin also caused translocation of GLUT4 molecules to the sarcolemma, and resulted in 61 +/- 2.6% of GLUT4 molecules on the sarcolemma. The combination of ischemia and insulin did not result in additive increases in sarcolemmal GLUT4 abundance. In more persistent or chronic ischemia, the other major myocardial glucose transporter, GLUT1, appears to play an important role. The mRNA for this transporter, which is constitutively expressed on cardiomyocyte sarcolemma, was increased 2.0-fold in regions of hibernating myocardium in humans with coronary heart disease as well as in persistently hypoxic rat neonatal cardiomyocytes in primary culture. In neither of these conditions was GLUT4 mRNA expression increased. Thus, acute myocardial ischemia increases sarcolemmal glucose transporter abundance mainly by translocating previously synthesized GLUT4 molecules from an intracellular compartment, whereas more chronic ischemia also increases GLUT1 abundance via enhanced mRNA expression. Increased GLUT1 and GLUT4 abundance may participate in the augmented glucose uptake of ischemic myocardium and therefore may help protect ischemic myocardium from irreversible injury.

Animals↗
PubMed1991

Cardiomyopathy: a necessary revision of the WHO classification.

The classification of myocardial disease proposed by the WHO/ISFC task force in 1980 distinguishes specific heart muscle diseases from myocardial diseases of unknown origin, termed cardiomyopathies, and differentiated into the dilated, hypertrophic and restrictive forms. This last group includes endomyocardiofibrosis and fibroblastic parietal endocarditis. In more recent years, two new forms of heart muscle disease have been recognized: so-called "primary" restrictive cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy. Primary restrictive cardiomyopathy is characterized anatomically by normally sized, non-hypertrophic ventricles with dilated atria, and functionally by impaired diastolic compliance due to myocardial stiffness. The clinical picture is that of chronic congestive heart failure; histology shows interstitial fibrosis and myocardial disarray, but not hypereosinophilia. In arrhythmogenic right ventricular cardiomyopathy, the myocardium of the right ventricular free wall is substituted by fibrous and/or adipose tissue, which results in regional dynamic alterations and ominous ventricular arrhythmias. The left ventricle is usually spared. Both forms should be classified as heart muscle diseases of unknown origin, and kept clearly distinct from the other cardiomyopathies listed in the WHO classification.

Arrhythmias, Cardiac↗
PubMed2000

[Is Na+Ca(2+) exchanger expression altered in the endomyocardium of patients with chronic heart valve diseases parallel to myocardial dysfunction?].

BACKGROUND: Na(+)-Ca2+ exchanger (EXCH) is an important regulator of intracellular calcium homeostasis. To maintain a normal intracellular Ca2+ concentration, EXCH expression may be upregulated before the onset of end-stage heart failure. We tested for a correlation between the EXCH transcription level and the degree of myocardial dysfunction as well as the suitability of EXCH transcription as a molecular marker for early detection of a transition from adequate to inadequate myocardial adaptation to chronic pressure and/or volume overload in valvular heart disease (VHD). METHODS: The level of EXCH transcription was analyzed in myocardial biopsies from eleven patients with aortic stenosis (AS), five with aortic regurgitation (AR) and six with primary mitral regurgitation (MR) of different hemodynamic severity and myocardial impairment using the quantitative rt-PCR technique. In addition, endomyocardial tissue from thirteen explanted hearts with end-stage heart failure and biopsies from seven individuals without heart disease were investigated. RESULTS: The mean level of EXCH transcription in patients with AS was: 1.8 +/- 1.4 amol/ng total RNA, with AR: 1.9 +/- 0.8 amol/ng and with MR: 2.2 +/- +2.1 amol/ng. This was not from different controls (2.6 +/- 1.2 amol/ng total RNA). However, in myocardium from end-stage heart failure, EXCH transcription was increased fourfold amounting to 8.9 +/- 1.9 amol/ng total RNA. No difference in the EXCH transcription was found in VHD with respect to the degree of myocardial dysfunction: cardiac index (CI) > 3.5 l/min/m2 (EXCH 1.4 +/- 1.1 amol/ng total RNA); CI 3.5-2.4 (EXCH 2.5 +/- 1.8); CI < 2.4 (EXCH 1.8 +/- 1.0); EF-angio > 50% (EXCH 1.9 +/- 1.8); EF-angio < or = 50% (EXCH 1.9 +/- 0.9); EF-RNV > 50% (EXCH 2.4 +/- 1.8), EF-RNV < or = 50% (EXCH 1.7 +/- 1.0). CONCLUSION: Myocardial EXCH transcription does not change parallel to the degree of myocardial dysfunction in VHD. Consequently, myocardial EXCH transcription does not appear to be suitable as a parameter indicating the transition from adequate to inadequate myocardial adaptation to chronic volume and/or pressure overload.

Adaptation, Physiological↗