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PubMed2006

Update for primary healthcare providers: recent statin trials and revised National Cholesterol Education Program III guidelines.

Statins produce large, clinically important beneficial effects on total low-density lipoprotein (LDL) cholesterol and triglycerides while raising high-density lipoprotein (HDL) cholesterol--each of which increases the risks for cardiovascular disease (CVD). In randomized trials of secondary and primary prevention, and their meta-analyses, statins confer statistically significant, clinically important reductions in myocardial infarction, stroke, and CVD death. In 2001, the National Cholesterol Education Program (NCEP) Adult Treatment Panel (ATP) III included LDL as the primary target, recommending optional goals of < 100 mg/dL for high-risk patients, < 130 mg/dL for moderate-risk patients, and < 160 mg/dL for low-risk patients. We conducted a search of randomized trials of statins whose results were published since May 15, 2001. We extracted overall trial results and data on adverse events, when available. We reviewed 7 published trials of statins, some of which contributed to the recent addendum to the NCEP ATP III guidelines that recommend reducing LDL goals to < 70 for very high-risk and < 100 for moderately high-risk patients via statins. Data from these trials demonstrate that greater LDL reductions produce larger CVD benefits in various categories of high- and moderate-risk patients, including a large number of primary prevention patients with metabolic syndrome who should be treated as aggressively as patients who have survived a myocardial infarction or stroke. Together, these recent statin trials and the NCEP ATP III revised guidelines, if implemented by primary healthcare providers, would result in many more patients receiving statins of proven benefit and reassuring adverse event profile.

Cardiovascular Diseases↗
PubMed2005

Antithrombotic therapy in hypertension: a Cochrane Systematic review.

Although elevated systemic blood pressure (BP) results in high intravascular pressure, the main complications of hypertension are related to thrombosis rather than haemorrhage. It therefore seemed plausible that use of antithrombotic therapy may be useful in preventing thrombosis-related complications of elevated BP. The objectives were to conduct a systematic review of the role of antiplatelet therapy and anticoagulation in patients with BP, to address the following hypotheses: (i) antiplatelet agents reduce total deaths and/or major thrombotic events when compared to placebo or other active treatment; and (ii) oral anticoagulants reduce total deaths and/or major thromboembolic events when compared to placebo or other active treatment. A systematic review of randomised studies in patients with elevated BP was performed. Studies were included if they were >3 months in duration and compared antithrombotic therapy with control or other active treatment. One meta-analysis of antiplatelet therapy for secondary prevention in patients with elevated BP reported an absolute reduction in vascular events of 4.1% as compared to placebo. Acetylsalicylic acid (ASA) did not reduce stroke or 'all cardiovascular events' compared to placebo in primary prevention patients with elevated BP and no prior cardiovascular disease. Based on one large trial, ASA taken for 5 years reduced myocardial infarction (ARR, 0.5%, NNT 200 for 5 years), increased major haemorrhage (ARI, 0.7%, NNT 154), and did not reduce all cause mortality or cardiovascular mortality. In two small trials, warfarin alone or in combination with ASA did not reduce stroke or coronary events. Glycoprotein IIb/IIIa inhibitors as well as ticlopidine and clopidogrel have not been sufficiently evaluated in patients with elevated BP. To conclude for primary prevention in patients with elevated BP, antiplatelet therapy with ASA cannot be recommended since the magnitude of benefit, a reduction in myocardial infarction, is negated by a harm of similar magnitude, an increase in major haemorrhage. For secondary prevention in patients with elevated BP, antiplatelet therapy is recommended because the magnitude of the absolute benefit is many times greater. Warfarin therapy alone or in combination with aspirin in patients with elevated BP cannot be recommended because of lack of demonstrated benefit. Further trials of antithrombotic therapy are required in patients with elevated BP.

Aspirin↗
PubMed2006

[Fetal haemodynamic and left heart dysfunction].

Foetal cardiology is a well established field of paediatric cardiology. It is no longer a simple exercise of prenatal diagnosis of cardiac malformations. It also covers the investigation and treatment of arrhythmias and functional and dynamic cardiocirculatory evaluation of the foetus which does not always have primary organic cardiac disease. It is this aspect which will be described in this article. The interactions of the left heart / foetal haemodynamics are classified in two main groups according to whether the left myocardial dysfunction is primary or secondary to changes of pre- or afterload. The haemodynamics singularities of the normal foetal circulation are and essential basis for the understanding of the phenomena observed.

Arrhythmias, Cardiac↗
PubMed2000

Rationale, design, and baseline characteristics of a trial of prevention of cardiovascular and renal disease with fosinopril and pravastatin in nonhypertensive, nonhypercholesterolemic subjects with microalbuminuria (the Prevention of REnal and Vascular ENdstage Disease Intervention Trial [PREVEND IT]).

This study describes the rationale, design, and baseline characteristics of a trial to determine whether treatment with fosinopril 20 mg/day and/or pravastatin 40 mg/ day will prevent cardiovascular and renal disease in nonhypertensive (RR <160/100 mm Hg and not using antihypertensive medication) and nonhypercholesterolemic (total cholesterol <8.0 or <5.0 mmol/L in case of previous myocardial infarction and not using lipid lowering medication) men and women with persistent microalbuminuria (urinary albumin excretion >10 mg/L once in an early morning spot urine and 15 to 300 mg/24-hour at least once in two 24-hour urine collections). The Prevention of REnal and Vascular ENdstage Disease Intervention Trial is a single-center, double-blind, randomized, placebo-controlled trial with a 2 x 2 factorial design. The 864 randomized subjects will be monitored for a minimum of 4 years and a maximum of 5 years. The primary efficacy parameter is defined as the combined incidence of all-cause mortality or hospital admission for documented (1) nonfatal myocardial infarction, (2) myocardial ischemia, (3) heart failure, (4) peripheral vascular disease, (5) cerebrovascular accident and/or (6) end-stage renal disease.

Adult↗
PubMed2002

Cardiovascular disease outcomes during 6.8 years of hormone therapy: Heart and Estrogen/progestin Replacement Study follow-up (HERS II).

CONTEXT: The Heart and Estrogen/progestin Replacement Study (HERS) found no overall reduction in risk of coronary heart disease (CHD) events among postmenopausal women with CHD. However, in the hormone group, findings did suggest a higher risk of CHD events during the first year, and a decreased risk during years 3 to 5. OBJECTIVE: To determine if the risk reduction observed in the later years of HERS persisted and resulted in an overall reduced risk of CHD events with additional years of follow-up. DESIGN AND SETTING: Randomized, blinded, placebo-controlled trial of 4.1 years' duration (HERS) and subsequent unblinded follow-up for 2.7 years (HERS II) conducted at outpatient and community settings at 20 US clinical centers. PARTICIPANTS: A total of 2763 postmenopausal women with CHD and average age of 67 years at enrollment in HERS; 2321 women (93% of those surviving) consented to follow-up in HERS II. INTERVENTION: Participants were randomly assigned to receive 0.625 mg/d of conjugated estrogens and 2.5 mg of medroxyprogesterone acetate (n = 1380), or placebo (n = 1383) during HERS; open-label hormone therapy was prescribed at personal physicians' discretion during HERS II. The proportions with at least 80% adherence to hormones declined from 81% (year 1) to 45% (year 6) in the hormone group, and increased from 0% (year 1) to 8% (year 6) in the placebo group. MAIN OUTCOME MEASURES: The primary outcome was nonfatal myocardial infarction and CHD death. Secondary cardiovascular events were coronary revascularization, hospitalization for unstable angina or congestive heart failure, nonfatal ventricular arrhythmia, sudden death, stroke or transient ischemic attack, and peripheral arterial disease. RESULTS: There were no significant decreases in rates of primary CHD events or secondary cardiovascular events among women assigned to the hormone group compared with the placebo group in HERS, HERS II, or overall. The unadjusted relative hazard (RH) for CHD events in HERS was 0.99 (95% confidence interval [CI], 0.81-1.22); HERS II, 1.00 (95% CI, 0.77-1.29); and overall, 0.99 (0.84-1.17). The overall RHs were similar after adjustment for potential confounders and differential use of statins between treatment groups (RH, 0.97; 95% CI, 0.82-1.14), and in analyses restricted to women who were adherent to randomized treatment assignment (RH, 0.96; 95% CI, 0.77-1.19). CONCLUSIONS: Lower rates of CHD events among women in the hormone group in the final years of HERS did not persist during additional years of follow-up. After 6.8 years, hormone therapy did not reduce risk of cardiovascular events in women with CHD. Postmenopausal hormone therapy should not be used to reduce risk for CHD events in women with CHD.

Aged↗
PubMed2000

[Evidence of the efficacy of hypocholesterolemic treatment in primary and secondary prevention of ischemic heart disease].

Good clinical medicine is, nowadays, not based on personal experiences, but in the results of broad prospective controlled studies considering the experience of many professionals, which in the case of new therapeutic options are named clinical trials. Several evidences of the determinant role of cholesterol in the development of atherosclerosis are reviewed. Pathologic studies illustrate the presence of cholesterol in atheroma plaques, with a good correlation between the severity of lesions and the amount of cholesterol in the plaques. Animal experiences demonstrate that hypercholesterolemia, rarely spontaneous, usually induced with dietary modifications, induces atherosclerosis in animals. Observation of patients with genetic-based hypercholesterolemia shows a high frequency of coronary atherosclerosis among them, and the broad cohort studies corroborate a good correlation between cholesterolemia and coronary heart disease. Finally, hypolipidemic intervention trials, mainly with drugs, and specially with statins, have clearly defined the benefits in coronary risk reduction.

Aged↗
PubMed1998

[Myocardial ischemia and ventricular arrhythmia].

A relation between myocardial ischemia and induction of ventricular arrhythmias can be demonstrated in patients with coronary heart disease--in contrast to patients with primary non ischemic cardiac diseases--using a combined metabolic-electrophysiological investigation protocol consisting of programmed atrial and ventricular stimulation with simultaneous measurement of the arterio/coronary venous difference for lactate, pyruvate, free fatty acids and amino acids. There are significant metabolic distinctions between both ischemic and non ischemic heart disease under pacing stress conditions as well as at rest. Areas of "hibernating myocardium" resp. "mismatch" zones in the myocardium showing reduced or abolished perfusion and preserved metabolism during scintographic SPECT/PET studies, may be found more often in patients with ventricular tachycardias (VT) or ventricular fibrillation (VF) in the chronic post myocardial infarction state than in patients without VT/VF. The proof of such zones may be considered a possible risk factor for arrhythmic events and sudden cardiac death after myocardial infarction. Hereby the concept of an interaction between acute and chronic ischemia triggering the onset of polymorphic VT or VF gaines increasing acceptance. In contrast, monomorphic reentrant VT are usually generated in the border zone of scarred areas where islands of vital fibers are surrounded by fibrotic tissue. These arrhythmogenic origin regions are characterized by a "match" pattern presenting a comparably severe reduction of perfusion and metabolism. Under those circumstances a control resp. suppression of the VT focus can only be provided by interventional techniques like catheter ablation, antitachycardiac surgery or implantation of a cardioverter/defibrillator beyond antiarrhythmic drug therapy. An antiischemic causal treatment (bypass surgery or angioplasty) represents for maximal 40% of patients with ischemically induced ventricular arrhythmias an adequate and sufficient therapeutic option. This pure antiischemic procedure seems to be justified especially in patients with preserved left ventricular function, proof of reversible ischemia and non inducibility of VT/VF following revascularization or non inducibility pre- and post intervention. In all other instances an additional treatment by antiarrhythmic drugs or preferably the implantable defibrillator is required.

Animals↗
PubMed1999

Cholesterol-lowering drugs. Some drugs with demonstrated efficacy but different benefits in primary and secondary prevention.

(1) In primary prevention trials, pravastatin and lovastatin prevented myocardial infarction and had a positive risk-benefit ratio in men with LDL-cholesterol values exceeding 4.5 mmol/l (1.7 g/l). Cholestyramine and gemfibrozil also prevented myocardial infarction in men with more severe hypercholesterolaemia; while clofibrate had a negative risk-benefit ratio in patients with moderate hypercholesterolaemia. These treatments have not been assessed for primary prevention in women or in patients aged over 70. (2) In trials involving patients with coronary heart disease, pravastatin and simvastatin both reduced the risk of myocardial infarction and/or mortality in patients of both sexes with LDL-cholesterol values above 3.2 mmol/l (1.2 g/l). Gemfibrozil also reduced the risk of myocardial infarction but not mortality, while clofibrate and bezafibrate had no preventive effect.

Anticholesteremic Agents↗
PubMedDate not supplied

Changing patterns of disease in Papua New Guinea over a period of 40 years from 1962. Pathology encountered in a stoneage culture by the first western-trained doctors who entered the country.

The diseases observed in Papua New Guinea coastal and highland people were described: segmental enteritis necroticans caused by the ingestion of pig meat contaminated with Clostridium welchii type C; chest empyemas caused by thoracostomies performed by village doctors because of ancient superstition; traumatic injuries; primary and secondary (lepromatous leprosy or tuberculosis) amylosis; slow prominent atherosclerosis and myocardial infarction.

Amyloidosis↗
PubMed1995

Comparison of thallium-201 resting redistribution with technetium-99m-sestamibi uptake and functional response to dobutamine for assessment of myocardial viability.

BACKGROUND: 201Tl scintigraphy is useful for determination of viability in patients with coronary artery disease and depressed left ventricular function. Whether 99mTc sestamibi is adequate for viability detection remains controversial. The primary goal of this study was to compare 99mTc-sestamibi uptake with 201Tl uptake in canine models of sustained low flow and regional asynergy for determination of viability. A secondary objective was to compare myocardial uptake of these tracers with the functional response to low-dose dobutamine. METHODS AND RESULTS: In protocol 1, 14 open-chested, anesthetized dogs with a 50% reduction in resting left anterior descending coronary artery (LAD) flow underwent 1 hour of transient LAD occlusion followed by reperfusion through the severe stenosis. Then 1.0 mCi of 201Tl was injected, and serial imaging was performed 5 minutes and 2 hours later. After acquisition of the delayed 201Tl image, 10 mCi of 99mTc sestamibi was injected, and imaging was repeated 45 minutes later. No significant difference was seen between the 201Tl defect ratio (LAD/left circumflex coronary artery [LCx]) on redistribution images (0.62 +/- 0.02) and 99mTc-sestamibi defect ratio (0.60 +/- 0.02). Similarly, LAD/LCx activity ratios by gamma-well counting were comparable (0.62 +/- 0.02 versus 0.59 +/- 0.04) and reflected the flow decrement. Systolic thickening was -11 +/- 3% at the time of tracer injection. In protocol 2, 16 dogs underwent serial 201Tl and 99mTc-sestamibi imaging during a 50% reduction in LAD flow with no superimposed transient LAD occlusion. In this model, the 99mTc-sestamibi LAD/LCx image defect ratio (0.61 +/- 0.03) was significantly less than the 201Tl redistribution image defect ratio (0.66 +/- 0.03, P < .01). In 10 dogs, the stenosis was released, resulting in a significant increase in systolic thickening (P = .003), which increased further in response to 5 micrograms.kg-1.min-1 of dobutamine (P = .02). In contrast, thickening increased only from -7 +/- 3% to 2 +/- 4% (P = .004) in response to dobutamine infusion in the remaining 6 dogs with persistent severe LAD stenoses. In protocol 3, 5 dogs received both 201Tl and 99mTc sestamibi to compare the degree of delayed redistribution between tracers at 2 hours. The LAD/LCx microsphere flow ratios when 201Tl and 99mTc sestamibi were injected were 0.44 +/- 0.06 and 0.43 +/- 0.05 (P = NS), respectively. The LAD/LCx activity ratio by gamma-well counting was greater for 201Tl (0.56 +/- 0.08) than 99mTc sestamibi (0.50 +/- 0.07) at 2 hours of redistribution (P < .05), indicating greater redistribution for 201Tl. The LAD/LCx 99mTc-sestamibi defect ratios on serial imaging improved from 0.49 +/- 0.07 to 0.52 +/- 0.07 (P = .0005), consistent with a slight amount of 99mTc-sestamibi redistribution. In protocol 4, no difference between 201Tl and 99mTc-sestamibi defect magnitudes was seen in 4 dogs undergoing 3 hours of total LAD occlusion and ligation of visible coronary collaterals. Infarct size was 68 +/- 19% of the risk area. CONCLUSIONS: Although 99mTc-sestamibi and 201Tl defect magnitudes and regional activities were comparable in dogs with sustained low coronary flows and superimposed subendocardial infarctions and in dogs with large infarctions, approximately 5% more 201Tl than 99mTc-sestamibi uptake was observed in dogs with chronic low flow and severe systolic dysfunction. Substantial 99mTc-sestamibi uptake in asynergic zones was observed in this low-flow model, with some slight resting 99mTc-sestamibi redistribution observed on serial images. Systolic thickening was negligibly enhanced during dobutamine infusion in dogs with sustained low flow, whereas 201Tl uptake was only mildly reduced.

Animals↗
PubMed2003

Randomized, double-blind, placebo-controlled, international trial of the oral IIb/IIIa antagonist lotrafiban in coronary and cerebrovascular disease.

BACKGROUND: This is the primary report of the large-scale evaluation of lotrafiban, an orally administered IIb/IIIa receptor antagonist, a unique trial with respect to the platelet antagonist, protocol design, and inclusion of cerebrovascular disease in a significant proportion of patients. METHODS AND RESULTS: Patients with vascular disease were randomized to lotrafiban 30 or 50 mg BID on the basis of age and predicted creatinine clearance or placebo in addition to aspirin at a dose ranging from 75 to 325 mg/d at the discretion of the physician-investigator. Follow-up was for up to 2 years. The primary end point was the composite of all-cause mortality, myocardial infarction, stroke, recurrent ischemia requiring hospitalization, and urgent revascularization. Of 9190 patients enrolled from 23 countries and 690 hospitals, 41% had cerebrovascular disease at the time of entry, and 59% had coronary artery disease. Death occurred in 2.3% of placebo-assigned patients and 3.0% of lotrafiban-group patients (hazard ratio 1.33, 95% CI 1.03 to 1.72, P=0.026), and the cause of excess death was vascular related. There was no significant difference in the primary end point (17.5% compared with 16.4%, respectively; hazard ratio 0.94, 95% CI 0.85 to 1.03, P=0.19). Serious bleeding was more frequent in the lotrafiban group (8.0% compared with 2.8%; P<0.001). Serious bleeding was more common among patients who received higher doses of aspirin (>162 mg/d), with or without lotrafiban. CONCLUSIONS: Lotrafiban, an orally administered platelet glycoprotein IIb/IIIa blocker, induced a 33% increase in death rate, which was vascular in origin and not affected by the type of atherosclerotic involvement at entry to the trial. Although the dose of aspirin was not randomly assigned, the finding of increased bleeding with doses >162 mg/d is noteworthy.

Administration, Oral↗
PubMed1975

Left-axis deviation: etiologic factors in one-hundred patients.

Clinical and electrocardiographic findings were analyzed in 100 consecutive cases of LAD. Below the age of forty years, LAD was uncommon, but its incidence increased continuously thereafter. The most frequent primary clinical diagnosis was arteriosclerotic heart disease. The functional mechanism producing LAD most often was LAHB, responsible in about 40 per cent. Approximately half the instances of LAHB were associated with old myocardial infarction of septal, anterior, or lateral regions, but half were seen in the absence of infarction or clinical coronary sclerosis and are presumed due to primary degenerative processes within these specialized conducting fibers. Approximately one-sixth of the instances of LAD were due to loss of inferior forces following inferior myocardial infarction. Typical left ventricular hypertrophy was a distinctly uncommon cause of LAD. Last, in 24 patients with LAD the mechanism or cause was not evident initially, of which two were subsequently shown to represent a very mild degree of LAHB. Also it is suggested that asymmetric myocardial hypertrophy of the anterior wall may account for some instances of LAD not otherwise explained.

Adult↗
PubMed1991

Cardiac changes implicated in chronic heart block.

Fifteen cases of chronic heart block were studied. Eight of them could be designated as idiopathic or primary heart block; the others were associated with hypertension, diabetes and ischaemic heart disease, either singly or in various combinations. In six cases, the whole heart was available for histopathological study of the conduction system. In the other 9 cases, only a portion of the heart muscle was available for examination. A V nodal fibrosis extending upto the proximal bundle of His was seen in all the six whole heart autopsy materials. Fibrosis of the adjacent myocardium was seen in five cases. In three cases, conducting system fibrosis was associated with atherosclerotic (1 case) or diabetic changes (3 cases) of the intramural vessels. In the 9 partial autopsy studies, myocardial fibrosis was seen in two cases, diabetic microangiopathy in one and atherosclerotic changes in two including an old thrombus in one. Thus, diabetic microangiopathy was seen in total four cases. These changes may be responsible for the cardiomegaly and cardiac failure associated with conduction defects observed in diabetes. In the idiopathic group also, heart block could be considered as a significant facet of a primary myocardial degenerative process.

Chronic Disease↗
PubMedDate not supplied

Prospective observational study of primary angioplasty of the infarct-related artery for acute myocardial infarction.

Primary angioplasty has been shown to reduce rates of in-hospital mortality, recurrent ischaemia and infarction. However, the role of primary stenting and abciximab is presently undergoing evaluation. This study attempted to examine the feasibility, safety and outcomes of primary angioplasty in the treatment of acute myocardial infarction. Data in 100 patients who underwent primary angioplasty for evolving acute myocardial infarction was prospectively analysed to assess the safety and efficacy of various modalities. Twenty patients were in Killip class III and above. Multivessel (2 or more vessels) disease was noted in more than 52 cases. Procedural success was 99 percent; 86 patients received primary stenting, majority of them had Kalam-Raju stent implantation. Adjunct treatment included abciximab infusion in 22 and intra-aortic balloon pump support in 12. Overall mortality rate was six percent with a mortality of 2.2 percent in non-cardiogenic shock patients. Recurrent ischaemic events were noted in five, three of them had successful reperfusion with repeat angioplasty. None of the patients had emergency coronary artery bypass surgery. It is concluded that primary angioplasty is safe and effective with high procedural success. Recurrent ischaemic events are low, possibly due to routine use of stenting and selective use of abciximab.

Abciximab↗
PubMed1997

An expert system for diagnosis of acute myocardial infarction with ECG analysis.

Coronary heart disease is one of the most prevalent and costly health care problems in the world. The early and accurate diagnosis of coronary heart disease is a major problem in emergency settings. However, many primary and secondary hospitals and primary emergency units lack cardiologists on call which makes the diagnosis difficult. This paper describes an expert system for diagnosis of acute myocardial infarction developed to aid physicians without cardiology specialization. Our main goal was to develop an expert system that assists in the diagnosis and indicates the need of hospitalization in a coronary unit.

Electrocardiography↗
PubMed2005

Increased myocardial N-myristoyltransferase activity in rotenone model of Parkinsonism.

There is widespread brain pathology in Parkinson's disease (PD), with the primary pathology in the substantia nigra. Oxidative stress is believed to play a role in cell death in PD. Rotenone is a mitochondrial toxin which can produce Parkinson syndrome (PS) in rats. Myristoyl-CoA:protein N-myristoyltransferase (NMT), which catalyzes the co-translational transfer of myristate from myristoyl-CoA to the amino-terminal glycine residue of selected polypeptides, is increased in the myocardium of ischemia-reperfusion rat model myocardium. Animals received rotoneone (n=10) or placebo vehicle (n=6) via Alzet osmotic pumps. Mean cardiac muscle NMT activity of placebo treated (control) rats was 0.608+/-0.366 units/mg protein. Rats with mild or no detectable PS features on rotenone showed slight (mean 0.853+/-0.192) but insignificantly increased activity. Rats that had moderately severe PS features had higher level of NMT activity (mean 1.223+/-0.057), which was borderline significant compared to controls (P=0.066). Rats with severe PS features had the highest NMT activity (1.353+/-0.128) which was significantly greater compared to controls (P=0.003) and to the rats that had equivocal or no motor slowing (P=0.005). Our data show cardiac metabolic dysfunction in a rotenone rat model of PS. The severity of this change correlates with the severity of motor manifestations. Further studies of NMT activity in human PD cases and patients with cardiomyopathy of unknown cause may provide valuable information in these disorders.

Acyl Coenzyme A↗
PubMed1991

Mechanical ventilation considerations in complex congenital heart disease.

It is the philosophy of our institution to provide primary surgical repair of complex congenital heart defects to avoid pulmonary and myocardial damage that occurs over time. Application of knowledge of the normal physiology and a clear understanding of the physiologic alterations of complex lesions are essential in understanding the effect of positive-pressure ventilation in complex CHD. The care and management of patients with CHD have a great deal to do with ventilatory management, which can be life-threatening when not fully understood but lifesaving when mastered. A dedicated team approach enhances communication and collaborative practice, which provides optimal patient management and outcome.

Adult↗