SEARCH · PubMed Health

Results for “MYOCARDIAL DISEASES, PRIMARY”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 451 records · Page 25Linked to original sources

PubMed2005

Prospective evaluation of the relationship between C-reactive protein, D-dimer and progression of peripheral arterial disease.

OBJECTIVE: Elevated levels of C-reactive protein (CRP) and D-dimer (DD) have been associated with the presence and progression of various forms of atherosclerotic disease, particularly coronary heart disease. We hypothesize that there is a relationship between elevated levels of baseline CRP and DD and progression of peripheral arterial disease (PAD) in patients with symptomatic PAD. The current study is a prospective evaluation of this hypothesis. METHODS: Between 1996 and 2003, 384 subjects were enrolled in a National Institutes of Health-sponsored blinded, prospective trial evaluating the effects of multiple atherosclerotic risk factors on progression of symptomatic PAD. Baseline levels of CRP and D-dimer were obtained in 332 subjects. Subjects were followed every 6 months with clinical history and exam, ankle-brachial pressure index (ABI), and carotid artery duplex scanning (CDS). The primary study end point was a composite of ABI progression, CDS progression, stroke, myocardial infarction, amputation, and death from cardiovascular disease. Secondary end points included each of the components of the primary end point. The relationship between time to the various endpoints and baseline CRP and DD levels was examined by life-table analysis and Cox proportional hazards analysis. RESULTS: Adequate baseline samples for CRP and DD were available in 332 subjects (mean age, 67 years; 57.8% men) with mean follow-up of 38.4 months (range, 1 to 99 months). Mean baseline levels (+/- SD) for CRP were 0.8 +/- 1.14 (range, 0.03 to 13.0), and mean DD levels were 227.4 +/- 303.3 (range, 1.9 to 2744.8). Progression, as defined by the primary end point, occurred in 48.5% of subjects. Subjects with elevated CRP (highest tertile) were no more likely to have any of the progression end points than those with the lowest values (lowest tertile) (P = NS, log-rank test, for all comparisons). By univariate analysis, subjects with elevated DD (highest tertile) were significantly more likely to die from any cause compared with subjects with the lowest DD values (lowest tertile) (P = .03, log-rank test). They were, however, no more likely to reach any of the other progression end points, including the primary end point (P = NS, log-rank test for all other comparisons). Multivariate analysis showed that DD level was a significant independent variable associated with occurrence of myocardial infarction (hazard ratio, 2.3; P = .02). CONCLUSIONS: In subjects with symptomatic PAD, elevated baseline DD, a marker of thrombotic activity, was significantly associated with the occurrence of myocardial infarction. This study did not confirm a relationship between progression of PAD and baseline DD or CRP during the first 3 years. Baseline DD and CRP do not provide useful risk stratification in patients at high risk for progression of symptomatic PAD. Future studies should evaluate serial levels of these markers to assess their utility in predicting progression of symptomatic PAD.

Aged↗

PubMed2006

Clinical events in high-risk hypertensive patients randomly assigned to calcium channel blocker versus angiotensin-converting enzyme inhibitor in the antihypertensive and lipid-lowering treatment to prevent heart attack trial.

The Antihypertensive and Lipid-Lowering treatment to prevent Heart Attack Trial (ALLHAT) provides a unique opportunity to compare the long-term relative safety and efficacy of angiotensin-converting enzyme inhibitor and calcium channel blocker-initiated therapy in older hypertensive individuals. Patients were randomized to amlodipine (n=9048) or lisinopril (n=9054). The primary outcome was combined fatal coronary heart disease or nonfatal myocardial infarction, analyzed by intention-to-treat. Secondary outcomes included all-cause mortality, stroke, combined cardiovascular disease (CVD), end-stage renal disease (ESRD), cancer, and gastrointestinal bleeding. Mean follow-up was 4.9 years. Blood pressure control was similar in nonblacks, but not in blacks. No significant differences were found between treatment groups for the primary outcome, all-cause mortality, ESRD, or cancer. Stroke rates were higher on lisinopril in blacks (RR=1.51, 95% CI 1.22 to 1.86) but not in nonblacks (RR=1.07, 95% CI 0.89 to 1.28), and in women (RR=1.45, 95% CI 1.17 to 1.79), but not in men (RR=1.10, 95% CI 0.92 to 1.31). Rates of combined CVD were higher (RR=1.06, 95% CI 1.00 to 1.12) because of higher rates for strokes, peripheral arterial disease, and angina, which were partly offset by lower rates for heart failure (RR=0.87, 95% CI 0.78 to 0.96) on lisinopril compared with amlodipine. Gastrointestinal bleeds and angioedema were higher on lisinopril. Patients with and without baseline coronary heart disease showed similar outcome patterns. We conclude that in hypertensive patients, the risks for coronary events are similar, but for stroke, combined CVD, gastrointestinal bleeding, and angioedema are higher and for heart failure are lower for lisinopril-based compared with amlodipine-based therapy. Some, but not all, of these differences may be explained by less effective blood pressure control in the lisinopril arm.

Amlodipine↗

PubMed1990

Platelet inhibitor therapy. Agents and clinical implications.

Platelets are central to the pathophysiology of an array of vascular disorders. Current platelet-inhibitor drugs reduce platelet aggregation through one of three pathways but do not prevent initial platelet adhesion. The most extensive clinical experience is with aspirin, an irreversible inhibitor of cyclooxygenase. Aspirin is clinically effective and has few gastrointestinal side effects if used at a dosage of 150 to 300 mg per day. Large clinical trials have documented the benefits of aspirin in arterial thromboembolic disease. It is effective in the primary and secondary prevention of myocardial infarction, including patients with unstable angina; reduces the acute thrombotic complications of coronary angioplasty and revascularization surgery; and also reduces cerebral ischemic events in patients with cerebrovascular disease. Aspirin is less effective for thrombi arising from the venous system or intracardiac chambers, which respond well to anticoagulants. Dipyridamole and sulfinpyrazone are most effective at preventing thrombosis on prosthetic surfaces. Dipyridamole reduces emboli from mechanical prosthetic valves when combined with warfarin and, unlike aspirin plus warfarin, does not increase bleeding complications. Newer agents such as ticlopidine and the thrombin inhibitor, hirudin, appear promising but require further evaluation. Because thrombin plays a critical role in mechanisms of arterial thrombosis, its inhibition appears promising for future therapy.

Adult↗

PubMed1979

Determinants of ventricular defibrillation in adults.

Conventional defibrillators which stored no more than 400 J and used damped sine wave pulses defibrillated 240 of 253 (95%) episodes of ventricular fibrillation (VF) in 94 prospectively assessed resuscitations in 88 adults. Shocks of 80--240 J (under 3 J/kg) delivered to the chest wall defibrillated more often than higher energy levels. Defibrillation rate did not correlate with weight. Defibrillation was determined by the diagnosis and setting in which VF occurred. Patients with acute myocardial infarction (AMI) and primary VF or with coronary disease and no AMI defibrillated more easily than patients with AMI and secondary VF or with no coronary disease. VF in a terminal patient (agonal VF) defibrillated less often than VF in other clinical situations. Age, weight, delivered energy, duration of pulse wave, and duration of VF had little, if any, influence on rate of defibrillation. These data fail to support the use of more expensive, high-output defibrillators sold by 11 or 14 American manufactures.

Adult↗

PubMed1999

Relative importance of improved hospital treatment and primary prevention. Results from 20 years of the Myocardial Infarction Register, Göteborg, Sweden.

OBJECTIVE: To analyse to what extent declines in incidence and mortality of coronary artery disease can be attributed to improved hospital and post-hospital treatment in contrast to how much is due to primary prevention. DESIGN: A register for non-fatal and fatal myocardial infarction and sudden coronary death registered in in-hospital as well as out-of-hospital events between 1975 and 1994. SETTING: City of Göteborg, Sweden, with 450,000 inhabitants. RESULTS: Seventy-one per cent of the decline in attacks could be attributed to a decline in first infarctions. Of the decrease in coronary deaths, 63% was due to a decline in out-of-hospital mortality. Previous registrations for myocardial infarction were considerably more common amongst people who died in hospital (29%) than amongst those who died out-of-hospital (11-16%) or who survived an infarction (11-13%). Out-of-hospital resuscitation contributed to about half of the reduction in out-of-hospital mortality. Thus, most of the decline in incidence and about half of the decline in sudden coronary deaths was due to primary preventive measures. Population data on risk factors indicate a decline of 37% between 1963 and 1995 in coronary risk amongst consecutive cohorts of 50-year-old men in the community. CONCLUSION: Out-of-hospital resuscitation, treatment in coronary care units and post-infarct treatment improved considerably, but changes in primary risk factors were also of major importance for the decline in incidence and mortality.

Adult↗

PubMed1989

Prevention of coronary heart disease: some results from the Oslo secondary and primary intervention studies.

The increase in cardiac disease [fatal and nonfatal myocardial infarction (MI), and sudden death] in the post-war years in Norway, after the much lower incidence during the war, that coincided with high and low fat intakes, respectively, led to a trial in Oslo to determine whether lowering dietary fat intake would favorably influence occurrence of coronary heart disease (CHD). Dietary modification, which lowered serum cholesterol of men who had suffered a first-time MI, showed decreased reinfarction incidence and cardiac deaths as compared with a comparable group of controls. Another study of normotensive high-risk men (on the basis of serum cholesterol and smoking habits) showed that dietetic measures can be useful in preventing CHD.

Adult↗

PubMed2005

Drug eluting stents in interventional cardiology -- current evidence and emerging uses.

Intervention in coronary artery disease is an area of cardiology where novel drugs, in the form of drug-eluting stents (DES), are being used increasingly commonly. DES are used across the whole range of coronary intervention, from stable angina patients with single or multivessel disease, acute coronary syndromes and acute myocardial infarction (i.e. primary angioplasty). Most recently, they are being tested in a particularly challenging subset of patients, those experiencing symptoms due to restenosis within a previously stented area of vessel (in-stent restenosis, ISR). This article summarises the rationale for the use of DES, across all these areas, focussing specifically on the emerging results of trials and registries examining the effectiveness of DES in acute myocardial infarction (AMI) and ISR. Drug-eluting stents represent a significant shift in the use of locally-delivered drugs in interventional cardiology. On the basis of encouraging trial data, including in the specific areas of in-stent restenosis and myocardial infarction, their use is becoming extremely widespread in place of bare-metal (drug-free) stents. This change is happening despite their high costs, relatively short follow-up data and concerns of possible unwanted effects, because of the weight of evidence that they are superior in preventing restenosis in many patient groups. This reduction is highly significant in angiographic terms and, to a lesser degree, in the prevention of clinically important restenosis requiring revascularisation, but not clearly in terms of overall mortality.

Animals↗

PubMed2004

Myocardial perfusion imaging in pediatric cardiology.

Myocardial perfusion imaging (MPI) is an important procedure in pediatric cardiology in terms of evaluating myocardial ischemia, infarction and damage associated with various congenital or acquired heart diseases, such as Kawasaki disease, anomalous origin of the left coronary artery from the pulmonary artery and complete transposition of the great arteries after arterial switch surgery. This type of imaging can detect myocardial damage in the morphological right ventricle when it functions as a systemic pumping chamber in patients with complex congenital heart diseases after intra-cardiac repair. Myocardial perfusion imaging can also evaluate myocardial damage associated with primary or secondary cardiomyopathy in children. The magnitude of increased right ventricular uptake on MPI is a useful noninvasive means of estimating right ventricular pressure overload due to congenital heart or pulmonary diseases. This article reviews myocardial perfusion tracers and pharmacological stress tests used to diagnose heart conditions in children, and the current clinical roles of MPI in pediatric cardiology.

Adolescent↗

PubMed1989

Antithrombotic therapy in the primary prevention of acute myocardial infarction.

The high factor VII coagulant (VIIc) activity in men at high risk of coronary heart disease suggests that restoring normal hemostatic activity with appropriate oral anticoagulants might constitute effective primary prevention. A pilot study was therefore undertaken of a randomized, double-blind, placebo-controlled trial of long-term, low-dose warfarin therapy. Middle-aged men at high risk (mean VIIc 120% of standard) but without clinical coronary heart disease or contraindications to anticoagulants were randomized to warfarin or placebo. The initial warfarin dose (2.5 mg/day) was increased at intervals to lower VIIc to 70% of standard and increase the prothrombin time international normalized ratio to 1.6. The control participants received the same dose sequence of placebo. The pilot study confirmed the feasibility of the design, the absence of any increased risk of serious bleeding, and the high compliance and low withdrawal rate from randomized treatment. Accordingly, a full-scale thrombosis prevention trial has been launched, which, in addition to low-dose warfarin, includes a low-dose aspirin regimen (75 mg/day) in a factorial design. The aim of this trial is to produce a 30% reduction in coronary heart disease in 6,000 high-risk men aged 45 to 69 years. The men will receive either separate or combined therapy and will be followed up for 5 years. Evidence so far indicates that the risk of bleeding in those receiving combined therapy will be no higher than that in those taking aspirin alone.

Aged↗

PubMedDate not supplied

Left ventricular systolic wall stress as a primary determinant of myocardial oxygen consumption: comparative studies in patients with normal left ventricular function, with pressure and volume overload and with coronary heart disease.

Left ventricular dynamics, coronary blood flow (Vcor), and myocardial oxygen consumption (MVO2) were determined in normal patients (N), in chronic pressure overload (aortic stenosis, AS), in chronic volume overload (aortic incompetence, AI), and in coronary heart disease (CHD). Peak systolic and enddiastolic wall stress were increased in AS and AI by 26-52 per cent, the systolic stress being preferably increased in AS, whereas enddiastolic stress was markedly greater in AI. Vcor and MVO2 were elevated in both groups by 45-55 per cent (p less than 0.001). Sufficient correlation was present between peak systolic wall stress and the MVO2 (r equal to 0.82). Since at a given wall stress the MVO2 was somewhat increased in AI and AS when compared with N and CHD, the considerable inhancement of the rate of pressure development (AS) was well as of the external cardiac work (AI) may contribute to the increase in overall oxygen consumption. It is concluded that systolic wall stress represents a primary determinant of MVO2 in pressure and volume overload and that the MVO2 increases in these diseases when hypertrophy becomes inappropriate with regard to the pressure and volume demands imposed to the left ventricle.

Aortic Valve Insufficiency↗

PubMed1998

Cardiovascular triggers and morning events.

Sudden cardiac death, myocardial infarction, unstable angina, ventricular tachyarrhythmias, fatal pulmonary thromboembolism, rupture of thoracic aorta, and ischemic and hemorrhagic cerebrovascular accidents exhibit a prominent circadian pattern with events more frequently during the morning (0600-1200 h)after awakening. Hematologic processes (e.g. increases in secretion and aggregability of platelets, changes in blood clotting, and fibronolysis), vascular processes (e.g. increase in vascular tone), and hemodynamic processes (e.g. morning surge of blood pressure, secretion of catecholamines, and shear forces) have been implicated in onset of disease. The primary significance of the recognition of circadian variation in the onset of myocardial infarction at any time of the day. Several triggers of the onset of cardiovascular disease have been identified. These include the start of activity in the morning, sexual activity, anger, and heavy physical exertion. However, increasing levels of habitual physical activity have been associated with progressively lower relative risks for cardiovascular events. Through further epidemiologic, clinical, and basic scientific research, we may achieve a better understanding of the mechanisms s that provoke the onset of acute cardiovascular disease. This knowledge will help investigators to devise effective preventive treatments for acute cardiovascular disorders.

Journal Article↗

PubMed2000

Acute myocardial infarction in a patient with anomalous left coronary artery origin and primary antiphospholipid syndrome.

Anomalous left main coronary artery (LMCA) originating from the right coronary sinus and running between the aorta and pulmonary trunk is a rare congenital condition. Although this disease is known to be associated with myocardial infarction and sudden death, the precise mechanism is uncertain. A 14-year-old male with this anomaly developed myocardial infarction during exercise complicated by primary antiphospholipid syndrome. He was admitted to hospital with persistent chest pain and sudden cardiac collapse that occurred while he was running. Cardiac catheterization demonstrated a narrowed segment in the LMCA and impaired blood flow, prompting a diagnosis of extensive anterior myocardial infarction. Emergency bypass surgery was performed using a single saphenous vein graft to the left anterior descending artery. Postoperative angiography showed the presence of an anomalous LMCA arising from the right sinus of Valsalva and running between the great vessels. The aortic samples were pathologically normal. He was discovered to also have primary antiphospholipid syndrome and was discharged without symptoms after warfarin therapy. Complicated primary antiphospholipid syndrome may trigger myocardial infarction in asymptomatic patients with this type of coronary anomaly.

Acute Disease↗

PubMed2001

Bleomycin, lomustine, cyclophosphamide, vincristine, procarbazine and prednisone (BLEO-CCVPP) in patients with Hodgkin's disease who relapsed after radiotherapy alone: a long-term follow-up study of the Eastern Cooperative Oncology Group (E3481).

Thirty-three evaluable patients with Hodgkin's disease who failed radiotherapy were treated on this phase II study with bleomycin, lomustine, cyclophosphamide, vincristine, procarbazine and prednisone given every 28 days for a minimum of eight courses. Twenty-five patients (76%; 95% CI=55.6-87.1%) achieved a complete remission, the median duration of which cannot yet be determined, but the probability of remaining in continuous complete remission at 10 years is.64. The median survival from entry on this study for all evaluable patients is 10 years, and 12 patients were alive at the time of this analysis with a median follow-up for them of 15.5 years. Of the 22 patients who died, 11 died of progressive or recurrent Hodgkin's disease and 11 died of other causes including 7 second primary neoplasms and at least one myocardial infarction. Both are now well known late complications of Hodgkin's disease treatment.

Adolescent↗

PubMed1994

Acute myocardial infarction in a case of myelofibrosis with patent coronary arteries and arteriovenous fistulae draining into the main pulmonary artery.

Explore the source record for details and available documents.

Aged↗

PubMed2004

Calcium channel blockers in the treatment of hypertension and prevention of cardiovascular disease: results from major clinical trials.

The ability of antihypertensive agents such as ss-blockers and thiazide and thiazide-like diuretics to reduce the risk of cardiovascular disease is well documented. The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) was undertaken to determine whether the newer classes of antihypertensive drugs-namely, calcium channel blockers (CCBs), alpha-1 blockers, and angiotensinconverting enzyme (ACE) inhibitors-were as effective as the older agents in preventing cardiovascular events. The results of ALLHAT showed that the diuretic chlorthalidone, the CCB amlodipine, and the ACE inhibitor lisinopril were equally effective in preventing the primary outcome-fatal coronary heart disease or nonfatal myocardial infarction. However, chlorthalidone and lisinopril were more effective at preventing heart failure, whereas amlodipine and chlorthalidone were more effective than lisinopril at preventing stroke. The ALLHAT findings, as well as those of other large, randomized, controlled antihypertensive trials, confirm the value of lowering blood pressure as an approach to reducing the risk, incidence, and economic burden of cardiovascular disease.

Algorithms↗

PubMed2001

Prevention of disease with pharmaceuticals.

The idea that diseases such as cardiovascular disease and cancer can be prevented by taking a 'pill' is attractive to many people. Chemoprevention is an established method in the primary and secondary prevention of cardiovascular disease such as myocardial infarct and stroke. Clinical trials have demonstrated beyond reasonable doubt that both fatal and non-fatal coronary events and strokes can be prevented. Antihypertensive drugs have been shown to be effective through clinical trials in preventing myocardial infarctions, stroke and other cardiovascular morbidity and mortality. Statins are commonly used to lower the blood cholesterol concentration, and aspirin is widely used to prevent occlusive vascular disease. Aspirin and other non-steroidal antiinflammatory agents have shown promise in the chemoprevention of colorectal cancer. While observational epidemiological studies have consistently suggested that diets rich in antioxidants such as beta-carotene might be useful in preventing coronary heart disease and cancer, the published reports of randomized trials clearly indicate that beta-carotene supplements are of no value in persons of high risk for such conditions. Although the chemoprevention of cancer is decades behind that of cardiovascular disease, there is no reason to believe that progress in cancer chemoprevention will differ substantially from that in cardiovascular disease. Better understanding of the molecular steps critical to carcinogenesis should open new avenues for cancer chemoprevention.

Cardiovascular Diseases↗

PubMed2001

Aspirin intake and the use of serum ferritin as a measure of iron status.

BACKGROUND: Atherosclerosis, a primary cause of myocardial infarction (MI), is an inflammatory disease. Aspirin use lowers risk of MI, probably through antithrombotic and antiinflammatory effects. Because serum ferritin (SF) can be elevated spuriously by inflammation, reported associations between elevated SF, used as an indicator of iron stores, and heart disease could be confounded by occult inflammation and aspirin use if they affect SF independently of iron status. OBJECTIVE: We tested the hypothesis that aspirin use is associated with reduced SF. DESIGN: We used analysis of covariance to investigate the relation between SF and categories of aspirin use in 913 elderly participants aged 67-96 y in the Framingham Heart Study. RESULTS: After adjustment for sex, age, body mass index, smoking, alcohol use, concentrations of C-reactive protein and liver enzymes, white blood cell count, and use of nonaspirin nonsteroidal antiinflammatory drugs and other medications, subjects who took >7 aspirins/wk had a significantly lower (by 25%) geometric mean SF than did nonusers, who took <1 aspirin/wk (71 compared with 95 microg/L, respectively; P for trend = 0.004). This effect of aspirin on SF was more marked in diseased subjects than in healthy subjects (mean SF was 50% lower compared with 21% lower, respectively). CONCLUSIONS: Aspirin use is associated with lower SF. We suggest this effect results from possible increased occult blood loss and a cytokine-mediated effect on SF in subjects with inflammation, infection, or liver disease. The relations between aspirin, inflammation, and SF may confound epidemiologic associations between elevated SF, as an indicator of iron stores, and heart disease risk.

Aged↗