Incidence Of Fatal Myocardial Infarction Research Articles

Role of Coenzyme Q10 in Prophylaxis of Myocardial Infarction.

Introduction: Coenzyme Q10 (CoQ10) has a potential role in reducing the risk of myocardial infarction by slowing the progression of atherosclerosis and improving ischemia. In this study, we will assess the role of coenzyme Q10 in prophylaxis for reducing myocardial infarction and mortality related to myocardial infarction.Methods: This open-label two open placebo-controlled randomized clinical trial was conducted in a tertiary care hospital in Sukkur, Pakistan from April 2016 to September 2019. Eight hundred nighty-two (892) patients with clinically diagnosed and documented evidence of hypertension were enrolled in the study from the outpatient department. Participants were randomized into two groups by 1:1 ratio using an online randomizer software, Research Randomizer (https://www.randomizer.org/). Group A received 100 mg coenzyme Q10 daily (coenzyme Q10 group) in addition to standard therapy and group B received standard therapy only (placebo group).Results: Participants who received coenzyme Q10 had fewer incidence of non-fatal myocardial infarction over 12 months (5.4% vs 8.4%) with relative risk reduction of 2.92 (confidence interval 95%, 0.55-2.76). The number needed to treat to prevent one non-fatal myocardial infarction was 34. Participants who received coenzyme Q10 had fewer incidence of fatal myocardial infarction over 12 months (1.5% vs 3.1%) with relative risk reduction of 1.65 (confidence interval 95%, 0.39-3.69). Number needed to treat to prevent one fatal myocardial infarction was 60.Conclusion: According to this study, coenzyme Q10 reduced the incidence of fatal and non-fatal myocardial infarctions. Clinicians should consider adding coenzyme Q10 to the treatment regimen of high-risk patients of myocardial infarction. We suggest coenzyme Q10 may be an effective prophylactic agent in patients at risk of myocardial infarction and it may help in reducing burden on the health care system.

Long-Term Effects of the 2011 Japan Earthquake and Tsunami on Incidence of Fatal and Nonfatal Myocardial Infarction

This study aimed to examine the long-term effects of the 2011 Japan earthquake and tsunami on the incidence of fatal and nonfatal myocardial infarction (MI). In the present study, the incidence of 2 types of cardiac events was comprehensively recorded. The study area was divided into 2 zones based on the severity of tsunami damage, which was determined by the percentage of the inundated area within the residential area (<10%, low-impact zone and ≥10%, high-impact zone). The standardized incidence ratio (SIR) and 95% CI for both types of cardiac events during the disaster year and the postdisaster years were determined in each zone. During the 4-year period after the disaster, the SIRs for nonfatal MI did not change to a statistically significant extent in either zones. For fatal MI, the SIR was stable during the study period in the low-impact zone. However, in the high-impact zone, the SIR was significantly elevated in the disaster year of 2011 (1.80 [95% CI 1.32 to 2.28]), and this increase was sustained for the following 3years (2012, 2.06 [1.55 to 2.57]; 2013, 1.99 [1.49 to 2.48]; 2014, 2.12 [1.62 to 2.63]). The SIRs for fatal MI for the 4 postdisaster years in the municipal areas were significantly correlated with the percentage of the inundated area (r= 0.83; p <0.001) and the number of deaths due to the tsunami (r= 0.77; p <0.005) but not with the maximum seismic intensity (r= 0.43; p= 0.12). In conclusion, these results suggest that the devastating tsunami was associated with a continual increase in the incidence of fatal MI among disaster survivors.

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Identifying the Vulnerable Patient with Rupture-Prone Plaque

Atherosclerotic cardiovascular disease is the leading cause of morbidity and mortality in the United States, and the obesity epidemic combined with aging of the population seems destined to increase the burden of this disease. Traditional cardiovascular risk assessment accounts for <50% of the variability in risk in the United States. Therefore, better and more effective identification of persons at high cardiovascular risk is needed. Our understanding of atherosclerosis has shifted from a focal disease whose hallmark is symptoms caused by a severe stenosis to a systemic disease characterized by endothelial dysfunction (ED) and plaque inflammation, with the potential for rupture and thrombosis mainly in those with subcritical stenosis. Under the new paradigm, clinicians require updated strategies to better assess the quality of arterial plaque. Effective tools for primary and secondary prevention of heart attack and stroke include intensive lifestyle modification, blood pressure reduction, and lipid-modifying therapies. These interventions are now understood to decrease plaque inflammation and thereby promote plaque stability. Lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) appears to be a specific marker of plaque inflammation that may play a direct role in the formation of rupture-prone plaque. In contrast, traditional risk factors, lipid measurement, and most vascular imaging modalities do not directly assess the acute ischemic potential in the arterial wall. Measuring Lp-PLA(2) levels in human serum or plasma is noninvasive and relatively inexpensive. Lp-PLA(2) may provide additional clinically relevant information that shows which patients have a high level of atherosclerotic disease activity as manifested by vascular inflammation, ED, and increased risk for progression toward rupture-prone plaque.

Can n-3 PUFA reduce cardiac arrhythmias? Results of a clinical trial

Dietary n-3 polyunsaturated fatty acids (PUFA) derived from fatty fish or fish oil may reduce the incidence of lethal myocardial infarction and sudden cardiac death. This might be due to a prevention of fatal cardiac arrhythmias. So far, however, only few clinical data are available being adequate to define indications for an antiarrhythmic treatment with n-3 PUFA. In a randomized, double-blind, placebo-controlled study 65 patients with cardiac arrhythmias without coronary heart disease or heart failure were subdivided into 2 groups. One group ( n=33) was supplemented with encapsulated fish oil (3 g/day, equivalent to 1 g/day of n-3 PUFA) over 6 months. The other group ( n=32) was given 3 g/day of olive oil as placebo. In the fish oil group a decrease of serum triglycerides, total cholesterol, LDL cholesterol, plasma free fatty acids and thromboxane B 2 as well as an increase of HDL cholesterol were observed. Moreover, a reduced incidence of atrial and ventricular premature complexes, couplets and triplets were documented. Accordingly, higher grades of Lown's classification switched to lower grades at the end of the dietary period. No changes were seen in the placebo group. The data indicate an antiarrhythmic action of n-3 PUFA under conditions of clinical practice which might help to explain the reduced incidence of fatal myocardial infarction and sudden cardiac death in cohorts on a fish-rich diet or supplemented with n-3 PUFA. Further studies elucidating the possible link between the reduced incidence of cardiac arrhythmias and sudden cardiac death by dietary intake of n-3 PUFA are warranted.

Progression of coronary atherosclerosis relates to the onset of myocardial infarction in an animal model of spontaneous myocardial infarction (WHHLMI rabbits).

Recently, we developed myocardial infarction-prone WHHLMI rabbits from coronary atherosclerosis-prone WHHL rabbits (WHHLCA rabbits) by selective breeding. In this study, we examined the relation of atherosclerotic plaques to the onset of myocardial infarction. We examined myocardial lesions of 378 WHHL rabbits born between 1992 and 2000, and atherosclerosis lesions of 93 WHHLCA and 82 WHHLMI rabbits. The aortic lesions were evaluated as percent surface lesion area. The coronary lesions were evaluated as cross sectional narrowing using sections prepared at 500 or 1,000 microm intervals. Serum lipid levels were assayed with enzymatic methods. The cumulative incidence of fatal myocardial infarction between 11 and 35 months old was 90% in WHHLMI rabbits and 21% in WHHLCA rabbits, respectively. Selective breeding increased the serum cholesterol levels by about 200 mg/dl despite there being no changes in triglyceride levels. Aortic and coronary atherosclerosis progressed markedly in WHHLMI rabbits compared to WHHLCA rabbits. Especially, WHHLMI rabbits over 15 months old showed more than 90% cross sectional narrowing of the left circumflex arteries, main stem of the left coronary artery, and the origin portion of the right coronary artery. In addition, there were no gender differences in atherosclerotic lesions of both aortas and coronary arteries. In conclusion, the present study showed that marked progression of coronary atherosclerosis was probably associated with spontaneous development of myocardial infarction in WHHLMI rabbits.

Development of an animal model for spontaneous myocardial infarction (WHHLMI rabbit).

Coronary heart disease is the most common cause of death in developed countries. However, there are no suitable animal models that mimic spontaneous myocardial infarction in humans. In this study, we attempted to obtain a rabbit strain with spontaneous myocardial infarction by selective breeding of coronary atherosclerosis-prone Watanabe heritable hyperlipidemic (WHHL) rabbits, designated as WHHLMI rabbits. WHHLMI rabbits were characterized by the high incidence of fatal myocardial infarction at ages 11 to 35 months, being increased from 23% to 97% after the selective breeding. The ECG on WHHLMI rabbits showed a typical feature of myocardial infarction. Histological examination of hearts from suddenly deceased WHHLMI rabbits revealed old myocardial infarction accompanied by fresh myocardial lesions. The culprit coronary arteries exhibited severe atheromatous plaques (>90% lumen area stenosis), suggesting that coronary atherosclerosis is responsible for myocardial infarction observed in WHHLMI rabbits. In addition, the coronary plaques showed vulnerable features including macrophage-rich thin cap and large necrotic core. To the best of our knowledge, this is the first report of spontaneous myocardial infarction in rabbits, and it is suggested that this WHHLMI rabbit strain will be a useful animal model to study human myocardial infarction.

Estrogen replacement therapy in women with a history of breast cancer

Estrogens are known as potent mammary mitogen substances and are the major stimulus for the growth of hormone-dependent tumors and clearly implicated in the pathogenesis of breast cancer. Therefore it is a general belief that hormone replacement therapy (HRT) after breast cancer will increase the risk of developing recurrences, though there are no clear data available to support this suggestion. No prospective study with a large number of patients and a long treatment period was performed concerning this issue. On the other hand it may not be justifiable to withhold hormone replacement therapy from low-risk patients after menopause, knowing the benefits of this therapy concerning osteoporosis and cardiovascular advantages. Nevertheless, until appropriate clinical trials help to resolve this problem, non hormonal alternatives constitute the standard of care. One possible approach is to treat menopausal women who have had breast cancer symptomatically and avoid ERT unless absolutely necessary. The risk of cardiovascular diseases can be reduced with lifestyle. Tamoxifen has a beneficial effect on serum lipids and the intake for 5 years leads to a 50% reduction in the incidence of fatal myocardial infarction and a decrease in morbidity associated with ischaemic heart disease. Low doses of progestogen is effective for menopausal hot flushes . Tibolone reduces vasomotoric symptoms such as hot flushes and offers benefit on osteoporosis and has shown a significant reduction in high-density lipoprotein cholesterol. Whether replacing of estrogens is safe for patients after breast cancer remains uncertain. There is a need for a large controlled clinical trial to evaluate the safety and advantages of long time estrogen replacement in women treated for breast cancer.

What kind of cardiovascular alterations could be influenced positively by oral antidiabetic agents?

Since the first publication of the University Group Diabetes Programme in 1970 the possible deleterious cardiovascular effects of certain hypoglycaemic sulphonylurea products has been well known. In contrast, international knowledge of the advantageous cardiovascular effects of certain sulphonylurea compounds became available recently. Glibenclamide decreases the incidence of fatal myocardial infarction and the development of ventricular fibrillation in patients suffering from acute myocardial infarction. It also lowers the incidence of ventricular ectopic beats in digitalized patients compared with patients treated with other investigated sulphonylurea compounds. The survival of patients treated with glibenclamide, insulin or diet alone is longer after the first attack of angina pectoris or after first acute myocardial infarction compared with those on other investigated sulphonylurea therapy. Glibenclamide decreases arrhythmogenesis during acute myocardial infarction in rats and strophanthin cardiotoxicity in rabbits. Arterial blood pressure and myocardial contractile force are not influenced by glibenclamide whereas these parameters are increased by other investigated sulphonylurea compounds. Consequently, deleterious cardiovascular effects of certain hypoglycaemic sulphonylurea drugs may contribute to the high cardiovascular mortality rate in diabetes mellitus, partly due to the effect on membrane channels and partly due to independent cardiac and extracardiac actions. Finally, recent observations suggest that glimepiride has a more advantageous cardiovascular effect than glibenclamide.

Tamoxifen and endometrial cancer: from experiment to patient.

Tamoxifen, a nonsteroidal antiestrogen, is the treatment of choice for adjuvant therapy in breast cancer patients. It is currently used both as a palliative treatment for advanced disease and as an adjunct following surgery for node positive or negative disease (Jordan 1994). In addition, tamoxifen’s estrogen-like properties have been noted to reduce the incidence of fatal myocardial infarction (McDonald and Stewart 1991; Stewart and Everington 1992) and maintain bone density in postmenopausal patients (Love et al. 1992; Ward et al. 1993; Kristensen et al. 1994). These observations led to the concept of testing tamoxifen as a preventive agent in women with a high risk for breast cancer. Clinical trials that will each recruit about 20000 women volunteers are now proceeding in the United States, the United Kingdom and Italy (Powles et al. 1994; Vanchieri 1992; Fisher and Redmond 1991). However, in contrast to the beneficial effect on bones and lipids, the estrogenic actions of tamoxifen in the uterus have raised serious doubts about the safety of long-term therapy. Satyaswaroop et al. (1984) first described the partial stimulation by tamoxifen of a human endometrial carcinoma transplanted in athymic mice. Gottardis et al. (1988) cotransplanted a human breast carcinoma and a human endometrial carcinoma into athymic mice to determine whether tamoxifen would control the estrogen stimulated growth of both tumors. Tamoxifen inhibited the growth of the breast tumor but encouraged the growth of the endometrial carcinoma.KeywordsEndometrial CancerEndometrial CarcinomaTamoxifen TherapyPostmenopausal Breast Cancer PatientTamoxifen Treated PatientThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Potassium channels in the cardiovascular system

In vitro and in vivo studies suggest that opening of ATP-sensitive potassium channels following ischaemia enhances recovery of myocardial contraction, dilates blood vessels and has an antiarrhythmic effect. Different sulphonylurea compounds that block the ATP-sensitive potassium channels exert different effects on cardiac functions. Glibenclamide decrease, arrhythmogenesis during acute myocardial infarction in rats and reduces strophanthin cardiotoxicity in rabbits. Other sulphonylurea compounds, but not glibenclamide, increase arterial blood pressure and myocardial contractility. These effects may be partly secondary to blockade of ATP-sensitive potassium channels and partly due to independent cardiac and extracardiac actions. Glimepiride may have a more advantageous cardiovascular effect than glibenclamide. The studies suggest the hypothesis that deleterious cardiovascular effects of some hypoglycaemic sulphonylurea drugs may contribute to the high cardiovascular mortality rate in diabetes mellitus. An observational study suggested glibenclamide decreased the incidence of fatal myocardial infarction and development of ventricular fibrillation in patients suffering from acute myocardial infarction. Glibenclamide may also decrease the incidence of ventricular ectopic beats in digitalized patients compared with other sulphonylurea compounds. The studies suggested the survival of subjects treated with glibenclamide, insulin, or diet alone after the first attack of angina pectoris or after first acute myocardial infarction may be longer compared with those on other sulphonylurea therapies. Further large scale prospective, randomised studies are needed to determine whether the reported effects can be verified and are sufficiently large to affect clinical prescribing.

Fatal myocardial infarction in the Scottish adjuvant tamoxifen trial. The Scottish Breast Cancer Committee.

To investigate the incidence of fatal myocardial infarction in women in the two randomised arms of the Scottish adjuvant tamoxifen trial. Retrospective review of hospital notes to determine with the greatest possible certainty women who had died of an acute myocardial infarction. Scottish Cancer Trials Office, the University of Edinburgh. 1070 postmenopausal women with operable breast cancer who were randomised to receive either adjuvant tamoxifen for five years or until relapse (539 patients) or tamoxifen for at least six weeks on the confirmation of first recurrence (531 patients). Incidence of fatal myocardial infarction in women with no known or suspected systemic cancer. Of the 200 women who died in the adjuvant tamoxifen arm of the trial, 44 were free of cancer at death and 10 of these died of myocardial infarction. In the observation arm 251 women died, of whom 61 showed no evidence of systemic cancer and 25 had a fatal myocardial infarction. The incidence of fatal myocardial infarction in the two groups was significantly different (chi 2 = 6.88, p = 0.0087). Tamoxifen given for at least five years as adjuvant therapy for breast cancer seems to have a cardioprotective oestrogen-like effect in postmenopausal women.

Clinical experience with preoperative coronary angiography.

CAD is the leading cause of postoperative and late death following peripheral vascular reconstruction. In an attempt to reduce the eventual incidence of fatal myocardial infarction, preoperative coronary angiography was obtained in a series of 1000 patients under serious consideration for elective vascular procedures at The Cleveland Clinic. Those patients found to have severe, surgically correctable CAD were advised to undergo myocardial revascularization as a combined or preliminary operation. Severe, correctable CAD was discovered in 25% of the study group, including 34% of patients suspected to have CAD by conventional clinical criteria in comparison to only 14% of those who were not (p = 2.0 X 10(-13) ). Although severe CAD also was more common among men, patients more than 60 years of age, and diabetic patients, the clinical cardiac status was the most reliable indication of the yield of coronary angiography. Coronary artery bypass was performed in 216 patients, and the operative mortality rate for 1292 cardiac and vascular procedures was 2.6%. On the basis of this experience, an algorithm was constructed to select peripheral vascular patients for noninvasive cardiac screening or coronary angiography.

Fatal myocardial infarction following carotid endarterectomy: three hundred thirty-five patients followed 6-11 years after operation.

Routine coronary angiography has been recommended to all patients undergoing carotid endarterectomy at the Cleveland Clinic since 1978. Patients found to have severe, correctable coronary artery disease (CAD) have been advised to undergo myocardial revascularization as a staged or combined procedure in conjunction with carotid endarterectomy in an attempt to reduce the incidence of fatal myocardial infarction during the postoperative period, and during the late follow-up interval. In order to provide an historic standard with which the results of this approach may eventually be compared, complete follow-up information has been obtained for 95% of 335 consecutive patients who underwent carotid endarterectomy between 1969 and 1973. Fatal myocardial infarction accounted for 60% of early deaths within 30 days of operation and occurred in 1.8% of the entire series. Among the patients who survived operation, the five-year mortality rate was 27%, and the 11-year mortality rate was 48%. Myocardial infarction caused 37% of the deaths that occurred within five years after operation and 38% of the deaths that have occurred within 11 years. Differences in the incidence of fatal myocardial infarction within five years after operation between a group of 116 patients who had no clinical evidence of CAD and a group of 209 patients suspected to have CAD attained statistical significance (p less than 0.1) despite the fact that 67 patients suspected to have CAD eventually underwent myocardial revascularization. Improvement in actuarial survival (p less than 0.05) and reduction in the late mortality rate (p less than 0.01) were statistically significant for the subset of patients with suspected CAD who had aortocoronary bypass graft procedures.