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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↗
PubMed1989

Stroke in the Lehigh Valley: racial/ethnic differences.

We investigated black/white differences in stroke rate (standardized morbidity), severity, and subtype, and the relative frequencies of 5 primary risk factors (hypertension, diabetes, myocardial infarction, other heart diseases, and transient ischemic attack [TIA]) using the Lehigh Valley Stroke Register. Blacks had a statistically significant higher, age-adjusted rate of stroke than whites. We found no differences in stroke severity using our measures but blacks had a statistically higher proportion of lacunar stroke, while whites had a higher proportion of embolic stroke. There were no differences in proportions of thrombotic stroke or intracerebral hemorrhage. The relative frequencies of hypertension, myocardial infarction, other heart diseases, and diabetes were higher for blacks, while the relative frequency of TIA was higher for whites. These observations are consistent with other reports that blacks have a higher frequency of stroke and tend to have more small-vessel cerebrovascular pathology than whites.

Age Factors↗
PubMed1978

Electrocardiographic manifestations and clinical significance of atrioventricular nodal alternating Wenckbach periods.

Atrioventricular nodal alternating Wenckebach periods were defined as episodes of 2:1 atrioventricular block in which there was a gradual increase in transmission intervals of conducted beats ending in two or three consecutively blocked atrial impulses. This is one of the mechanisms whereby 2:1 atrioventricular block progresses into 3:1 or 4:1 atrioventricular block. Alternating Wenckebach periods appear during rapid atrial pac,ng (even in the absence of depressed atrioventricular nodal function), provided that the atria can be captured at a rate fast enough to allow for the occurrence of this phenomenon. Treatment of atrial flutter with digoxin and quinidine produces alternating Wenckebach's periods, with associated electrocardiographic changes specific for the type of drug given. In patients with "atrial tachycardia with atrioventricular block" due to digitalis intoxication or with primary disease of the conducting system or with acute myocardial infarction, there are coexisting severe arrhythmias and clinical symptoms requiring almost immediate pharmacologic or electrical therapy. We conclude that atrioventricular nodal alternating Wenckebach's periods are common and frequentyly transient and that they occur in a variety of clinical conditions, most of which are benign; however, contrary to what is commonly accepted, some episodes appear in clinical settings requiring prompt pharmacologic or electrical treatment.

Acute Disease↗
PubMed2005

Costs and medical care consequences associated with the diagnosis of peripheral arterial disease.

BACKGROUND: Peripheral arterial disease (PAD) is increasingly recognised as an indicator of disseminated atherothrombosis, but its impact on use of healthcare resources is not well understood. OBJECTIVE: To provide a quantitative description of the resource utilisation and costs incurred following PAD. METHODS: Hospitalisations, physician visits and the corresponding direct medical costs were examined in 16,440 patients with a diagnosis of PAD (1985--1995) in Saskatchewan, Canada, and compared with 15,590 reference patients with a diagnosis of myocardial infarction (MI) [1990--1995]. Medical history and patient characteristics were available retrospectively to January 1980 and follow-up to December 2000. Rates and timing of all-cause and cardiovascular hospitalisations and physician visits within discrete periods in the 10 years following PAD diagnosis, and 5 years following MI, were evaluated, as were lengths of stay and predictors of hospitalisation. RESULTS: Average follow-up was 5.9 years among patients with PAD and 3.6 years for MI. Half (55%) of patients with PAD were male versus 64% of reference patients. The mean ages were 67.3 and 66.9 years, respectively. Patients with PAD were hospitalised most frequently soon after diagnosis, with rates subsequently decreasing to 0.14 per month. These rates were similar in the reference group except for the period immediately following MI. The average 5-year cost post-diagnosis (2002 Can dollars) per patient was 41,968 Can dollars vs 48,578 Can dollars for the reference population. CONCLUSIONS: A diagnosis of PAD not only imposes a severe burden on patients and their families, but it also significantly increases the use of healthcare resources and the associated costs. By the end of year 1, this burden is comparable with a diagnosis of MI.

Aged↗
PubMedDate not supplied

[Complement system proteins in the acute phase of myocardial infarction].

Content of C3 and C4 fractions was decreased in blood of patients with acute primary myocardial infarction within the first day of the disease as compared with the level of these fractions observed just after the hospitalization of the patients. These data suggest the activation of the complement system during this first period of the disease. The activation occurred mainly in the usual way as evidenced by single-directed alterations in content of C3 and C4 fractions. The activation of the complement system within the first day of the disease in apparently one of its pathogenetical manifestations. The experimental data are confirmed on participation of the complement system in development of early postischemic impairements of homeostasis.

Acute Disease↗
PubMed1995

Pharmacological modulation of cardiac fibroblast function.

The cardiac interstitium is composed of nonmyocyte cells and a structural protein network which plays a dominant role in governing the structure, architecture, and mechanical behavior of the myocardium. The heterogeneity in myocardial structure, created by the altered behavior of nonmyocyte cells, particularly cardiac fibroblasts which are responsible for myocardial collagen metabolism and fibrous tissue accumulation, may largely explain the appearance of diastolic and/or systolic myocardial failure. Regulatory mechanisms that are related to the fibrous tissue response in various cardiovascular diseases, e.g., hypertensive heart disease, dilated cardiomyopathy or post myocardial infarction, are of primary clinical interest. A better understanding of the hitherto neglected role of cardiac fibroblasts in mediating an adverse structural remodeling of the myocardium will lead to specific pharmacologic agents that interfere with the fibrous tissue response. Several lines of evidence based on in vivo and in vitro studies suggest that circulating and tissue renin-angiotensin-aldosterone systems (RAAS) are involved in the structural remodeling of the nonmyocyte compartment, including the cardioprotective effects of angiotensin converting enzyme (ACE) inhibition or aldosterone receptor antagonism that was found to prevent myocardial fibrosis in the rat with renovascular or genetic hypertension. In cultured adult cardiac fibroblasts, an angiotensin (Ang)II- or aldosterone-mediated dose-dependent increase in collagen synthesis could be completely abolished by the use of AngII type 1 or mineralocorticoid receptor antagonists, respectively. Likewise, the AngII-mediated decrease in the activity of matrix metalloproteinase 1, the key enzyme for interstitial collagen degradation, could be antagonized by AngII receptor blockade.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMed2005

A study of the pathology and pathogenesis of the myocardial lesions in gousiekte, a plant-induced cardiotoxicosis of ruminants.

Myocardial lesions were studied in sheep in which gousiekte was induced by experimental dosage of Pachystigma pygmaeum, Fadogia homblei or Pavetta harborii. The single most consistent diagnostic histological feature in 33 animals was hypertrophy of myocardial fibres in the subendocardial region. Fibrosis in the subendocardial region of the apex or left ventricular wall was often scarce or absent in animals with a short latent period, and was not always prominent even in sheep with an intermediate or long latent period. The presence or absence of fibrosis cannot therefore be used to confirm or exclude gousiekte, particularly in cases with shorter latent periods. Light microscopical and ultrastructural lesions in sheep with gousiekte correspond to a large extent to changes reported in humans with dilated cardiomyopathy of unknown cause. It appears that the myocardial lesions in gousiekte represent a final common pathway of cellular damage rather than a manifestation of a specific type of heart disease. The predilection for hypertrophy of myofibres in the subendocardial region is probably related to diminished perfusion that potentiates the primary myocardial dysfunction.

Animals↗
PubMed2004

[Statin therapy for hypertensive patients].

BACKGROUND: The majority of cardiovascular events and deaths attributable to both raised blood pressure and dyslipidaemia occur in subjects with relatively "normal" blood pressure and lipid levels respectively. The study was designed to evaluate the potential benefits of cholesterol lowering in the primary prevention of coronary heart disease in hypertensive subjects with average and below average levels of serum cholesterol. MATERIAL AND METHODS: Out of 19 342 hypertensive subjects (aged 40-79) who were initially randomized to one of two antihypertensive treatment strategies in the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT), 10 305 subjects with total cholesterol levels < or = 6.5 mmol/L were additionally randomized to either 10 mg atorvastatin or placebo. The primary endpoint was non-fatal myocardial infarction or fatal coronary heart disease. RESULTS: The lipid arm of the study was prematurely stopped after a median follow-up period of 3.3 years. One hundred events occurred in those randomized to atorvastatin compared to 154 events in those receiving placebo, a 36 % relative risk reduction (p = 0.0005) in the primary endpoint. Among secondary and tertiary endpoints, stroke was reduced with 27% (p = 0.02). There was a non-significant 13% reduction in total mortality. Non-cardiovascular mortality was similar in the two treatment limbs of the trial. After three years of follow-up, atorvastatin lowered total serum cholesterol by 1.1 mmol/L compared with placebo. INTERPRETATION: Treatment with 10 mg atorvastatin o.d. in hypertensive patients at moderate risk gives a significant risk reduction of coronary heart disease, independent of baseline level of total cholesterol.

Adult↗
PubMed2002

Effect of nicorandil on coronary events in patients with stable angina: the Impact Of Nicorandil in Angina (IONA) randomised trial.

BACKGROUND: In addition to its anti-ischaemic effects, the antianginal drug nicorandil is thought to have cardioprotective properties. We did a randomised trial to find out whether nicorandil could reduce the frequency of coronary events in men and women with stable angina and additional risk factors. METHODS: 5126 patients were randomly assigned 20 mg nicorandil twice daily (n=2565) or identical placebo (n=2561) in addition to standard antianginal therapy. The primary composite endpoint was coronary heart disease death, non-fatal myocardial infarction, or unplanned hospital admission for cardiac chest pain. The secondary endpoint was the combined outcome of coronary heart disease death or non-fatal myocardial infarction. Other outcomes reported include all-cause mortality, all cardiovascular events, and acute coronary syndromes. Mean follow-up was 1.6 years (SD 0.5). Analysis was by intention to treat. FINDINGS: There were 398 (15.5%) primary endpoint events in the placebo group and 337 (13.1%) in the nicorandil group (hazard ratio 0.83, 95% CI 0.72-0.97; p=0.014). The frequency of the secondary endpoint was not significantly different between the groups (134 events [5.2%] vs 107 events [4.2%]; 0.79, 0.61-1.02; p=0.068). The rate of acute coronary syndromes was 195 (7.6%) in the placebo group and 156 (6.1%) in the nicorandil group (0.79, 0.64-0.98; p=0.028), and the corresponding rates for all cardiovascular events were 436 (17.0%) and 378 (14.7%; 0.86, 0.75-0.98; p=0.027). INTERPRETATION: We showed a significant improvement in outcome due to a reduction in major coronary events by antianginal therapy with nicorandil in patients with stable angina.

Aged↗
PubMed2001

Challenges for the prevention of primary and secondary stroke: the importance of lowering blood pressure and total cardiovascular risk.

It is well established that blood pressure lowering is effective for the primary prevention of stroke and other cardiovascular disorders in subjects with blood pressures as low as 140/90 mmHg, and up to 80 years of age. Despite this knowledge, blood pressure levels are controlled in less than 25% of the hypertensive population worldwide. It has taken longer to prove that blood pressure lowering is equally effective for the prevention of recurrent stroke. The results of PROGRESS (Perindopril Protection Against Recurrent Stroke Study) have confirmed that a perindopril-based regimen in subjects with cerebrovascular disease substantially reduces the incidence of secondary stroke and primary myocardial infarction. It is daunting to recall that it has taken almost two decades for beta-blockers to be widely used for the secondary prevention of myocardial infarction, since widespread use of the PROGRESS regimen would prevent more than half a million strokes worldwide each year. The real challenge now is to implement novel and effective strategies for the control of blood pressure and other cardiovascular risk factors worldwide. Strategies should include lifestyle measures, such as stopping smoking, exercise and reducing overweight. There is a real need to identify hypertensive subjects and treat them with blood pressure lowering drugs for primary prevention. In subjects with established cardiovascular disease, consideration should be given to a range of proven interventions for secondary prevention, such as blood pressure lowering, irrespective of current blood pressure, anti-platelet drugs, statins for lowering cholesterol and glycaemic control in diabetics. Among new strategies to lower overall cardiovascular risk, consideration should be given to the development of single-pill combinations of drugs of known efficacy, including various combinations of ACE inhibitors, diuretics, beta-blockers, aspirin and statins, among others.

Antihypertensive Agents↗
PubMed2006

Myocardial perfusion defects in patients with autoimmune diseases: a prospective study. Analysis of two diagnostic tests.

A significant correlation between autoimmune diseases and premature or accelerated coronary atherosclerosis has been found. The objectives of the study were: (a) to evaluate myocardial perfusion defects in patients with autoimmune diseases by contrast echocardiography and nuclear imaging; and (b) to evaluate the prevalence of alterations in subclinical myocardial perfusion defects in autoimmune diseases. Myocardial perfusion in 37 patients was evaluated by contrast echocardiography at rest and with dobutamine and with nuclear imaging. The agreement between the two diagnostic tests at rest was 0.72 (P < 0.0001) and with dobutamine was 0.65 (P < 0.0001). The prevalence of abnormalities in myocardial perfusion in autoimmune diseases by contrast echocardiography and nuclear imaging was 27% and in patients with primary antiphospholipid syndrome was 30%. We concluded that there is a high level of agreement between contrast ecocardiography and nuclear imaging for assessment of myocardial perfusion defects in patients with autoimmune diseases, and their prevalence is similar to that reported in the literature.

Adolescent↗
PubMed1987

Radioiodine therapy of hyperthyroidism precludes thallium-201 myocardial scintigraphy.

The authors attempted to perform Tl-201 myocardial perfusion scintigraphy in a 42-year-old man 23 and 35 days after he received 9.8 mCi of oral I-131 for documented Graves' disease. Interference from primary and scattered photons from residual thyroid I-131 made Tl-201 myocardial scintigraphy technically impossible. A series of phantom and patient studies using I-131 and Tl-201 were performed, yielding guidelines for planning Tl-201 myocardial scintigraphy following radioiodine therapy.

Adult↗
PubMed1994

Aspirin in the primary prevention of cardiovascular disease.

The ability of aspirin to reduce cardiovascular disease risks has been tested in randomized trials in a wide range of patient categories. There are clear benefits of aspirin on nonfatal myocardial infarction, nonfatal stroke, and vascular death among patients with prior manifestations of cardiovascular disease, such as myocardial infarction, unstable angina, and stroke. Aspirin is also beneficial to those in the acute phase of evolving myocardial infarction. In primary prevention, there is a clear reduction in myocardial infarction in men. A large-scale primary prevention trial in women is presently underway.

Aspirin↗
PubMed2004

Kidney disease as a risk factor for recurrent cardiovascular disease and mortality.

BACKGROUND: Chronic kidney disease (CKD) is highly prevalent in the United States and is an independent risk factor for adverse cardiovascular disease (CVD) and all-cause mortality outcomes in patients with acute coronary syndromes. Few studies have evaluated the effect of CKD on cardiovascular events in a diverse community-based population with underlying CVD. METHODS: Data for subjects with preexisting CVD were pooled from 4 publicly available, community-based, longitudinal studies: Atherosclerosis Risk in Communities, Cardiovascular Health Study, Framingham Heart Study, and Framingham Offspring Study. CKD was defined as an estimated glomerular filtration rate less than 60 mL/min/1.73 m2 (<1 mL/s/1.73 m2). The primary study outcome was a composite of myocardial infarction (MI), fatal coronary heart disease (CHD), stroke, and all-cause mortality. The secondary outcome included only MI and fatal CHD. RESULTS: A total of 4,278 subjects satisfied inclusion criteria, and 759 subjects (17.7%) had CKD. Mean follow-up was 86 months. The primary and secondary outcomes were observed in 1,703 (39.8%) and 857 subjects (20.0%), respectively. Incidence rates for the primary and secondary outcomes were greater in persons with CKD compared with those without CKD (62.5% versus 34.9% and 30.6% versus 17.8%, respectively). Adjusted hazard ratios for the primary and secondary outcomes were 1.35 (95% confidence interval [CI], 1.21 to 1.52) and 1.32 (95% CI, 1.12 to 1.55), respectively. CONCLUSION: The presence of CKD in a community-based population with preexisting CVD is associated with an increased risk for recurrent CVD outcomes. This increased risk persists after adjustment for traditional CVD risk factors.

Aged↗
PubMed2005

Outcomes in hypertensive black and nonblack patients treated with chlorthalidone, amlodipine, and lisinopril.

CONTEXT: Few cardiovascular outcome data are available for blacks with hypertension treated with angiotensin-converting enzyme (ACE) inhibitors or calcium channel blockers (CCBs). OBJECTIVE: To determine whether an ACE inhibitor or CCB is superior to a thiazide-type diuretic in reducing cardiovascular disease (CVD) incidence in racial subgroups. DESIGN, SETTING, AND PARTICIPANTS: Prespecified subgroup analysis of ALLHAT, a randomized, double-blind, active-controlled, clinical outcome trial conducted between February 1994 and March 2002 in 33,357 hypertensive US and Canadian patients aged 55 years or older (35% black) with at least 1 other cardiovascular risk factor. INTERVENTIONS: Antihypertensive regimens initiated with a CCB (amlodipine) or an ACE inhibitor (lisinopril) vs a thiazide-type diuretic (chlorthalidone). Other medications were added to achieve goal blood pressures (BPs) less than 140/90 mm Hg. MAIN OUTCOME MEASURES: The primary outcome was combined fatal coronary heart disease (CHD) or nonfatal myocardial infarction (MI), analyzed by intention-to-treat. Secondary outcomes included all-cause mortality, stroke, combined CVD (CHD death, nonfatal MI, stroke, angina, coronary revascularization, heart failure [HF], or peripheral vascular disease), and end-stage renal disease. RESULTS: No significant difference was found between treatment groups for the primary CHD outcome in either racial subgroup. For amlodipine vs chlorthalidone only, HF was the only prespecified clinical outcome that differed significantly (overall: relative risk [RR], 1.37; 95% confidence interval [CI], 1.24-1.51; blacks: RR, 1.46; 95% CI, 1.24-1.73; nonblacks: RR, 1.32; 95% CI, 1.17-1.49; P<.001 for each comparison) with no difference in treatment effects by race (P = .38 for interaction). For lisinopril vs chlorthalidone, results differed by race for systolic BP (greater decrease in blacks with chlorthalidone), stroke, and combined CVD outcomes (P<.001, P = .01, and P = .04, respectively, for interactions). In blacks and nonblacks, respectively, the RRs for stroke were 1.40 (95% CI, 1.17-1.68) and 1.00 (95% CI, 0.85-1.17) and for combined CVD were 1.19 (95% CI, 1.09-1.30) and 1.06 (95% CI, 1.00-1.13). For HF, the RRs were 1.30 (95% CI, 1.10-1.54) and 1.13 (95% CI, 1.00-1.28), with no significant interaction by race. Time-dependent BP adjustment did not significantly alter differences in outcome for lisinopril vs chlorthalidone in blacks. CONCLUSIONS: In blacks and nonblack subgroups, rates were not lower in the amlodipine or lisinopril groups than in the chlorthalidone group for either the primary CHD or any other prespecified clinical outcome, and diuretic-based treatment resulted in the lowest risk of heart failure. While the improved outcomes with chlorthalidone were more pronounced for some outcomes in blacks than in nonblacks, thiazide-type diuretics remain the drugs of choice for initial therapy of hypertension in both black and nonblack hypertensive patients.

Aged↗