111 resultados para ISCHEMIC-HEART-DISEASE


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Ischaemic heart disease as the result of impaired blood supply is currently the leading cause of failure and death. Ischaemic heart disease refers to a group of clinicopathological symptoms including angina pectoris, acute myocardial infection, chronic ischemic heart disease, as well as heart failure and sudden cardiac death. Coronary artery ischemic heart disease, as well as heart failure and sudden cardiac death. Coronary artery thrombosis is the most common cause of acute myocardial infarction and sudden cardiac death. A thrombotic event is the result of two different processes: plaque disruption and endothelial erosion. The morphology of a "vulnerable plaque" is more clinically indicative than the plaque volume and the degree of luminal stenosis. However, identification of patients with vulnerable plaques remains very challenging and demands the development of new methods of coronary plaque imaging. Sudden death resulting from ventricular fibrillation or AV block frequently complicates coronary thrombosis, accounting for up to 50% of mortality.If a coronary artery is occluded for more than 20 min, irreversible damage to the pericardium occurs. Timely coronary recanalization and myocardial reperfusion limit the extent of myocardial necrosis, but may induce "reperfusion injuries", stunned myocardium, or reperfused myocardial hemorrhagic infarcts, all of which are related to infarct siz and coronary occlusion time. Reperfusion injuries have been described after cardiac surgery, percutaneous transluminal coronary angioplasty, and fibrinolysis. A prolonged imbalance between the supply of and demand for myocardial oxygen and nutrition leads to a subacute, acute, or chronic state (aka hibernating myocardium) of myocardial ischemia. Ischemic heart disease is bwelieved to be the underlying cause of heart failure in approximately two-thirds of patients, resulting from acute and/or chronic injury to the heart.

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For the past decade, PET and PET/CT have been widely studied for myocardial perfusion imaging. Several studies demonstrated the incremental value of PET for the diagnostic and prognostic assessment of patients with coronary artery disease. Moreover, PET allows for non-invasively quantifying myocardial blood flow and myocardial flow reserve, that both are recognized as surrogate marker of cardiac event free survival. By enabling the exploration of epicardial disease and the microvasculature, PET constitutes a unique tool to study pathophysiogical mechanisms leading to atherosclerosis genesis. The recent emergence of high-tech hybrid machines may even provide further incremental information about coronary function and morphology. By taking the best of each modality, a better assessment of patients with coronary artery disease is expected. (C) 2011 Elsevier Masson SAS. All rights reserved.

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The goal of this study was to assess the localization and types of thrombosed plaques in cases of sudden cardiac death attributed to coronary artery disease and to evaluate possible correlations with body mass index (BMI) and increased heart weight. This retrospective study was performed on forensic cases for which the cause of death was attributed to coronary artery disease. A complete autopsy and a multi-phase postmortem computed tomography (CT) angiography (MPMCTA) were performed in all cases. Eighty-five cases were selected (mean age, 55.18 ± 11.04 years; 72 men and 13 women). MPMCTA performed prior to autopsy enabled an evaluation of coronary artery perfusion before dissection of the body and helped therefore to guide sampling for histology. An acute coronary thrombosis was found in 57 cases, which included plaque erosion in 26 cases (mean age, 46.73 ± 8.33 years) and rupture or intra-plaque hemorrhage in 31 cases (mean age, 58.23 ± 10.62 years). Erosions were most frequently found in the left anterior descending artery (61.5 %), while only 35.48 % of ruptures were observed in this artery. Chronic coronary pathology was considered as the main cause of death in 28 cases (mean age, 59.64 ± 9.47 years). Sixty-two of the cases (72.94 %) had a BMI in the overweight category (BMI ≥25), with the highest mean BMI in patients with chronic coronary pathology without acute thrombosis found at autopsy. The heart weight was above the predicted reference values in 52 cases (61.18 %). Our results are in accordance with previously published studies on the spatial distribution of vulnerable plaques. We observed a higher percentage of eroded plaques than previously reported. Patients with coronary erosions were significantly younger than those with plaque rupture or those without an acute coronary thrombosis (p values <0.0001). BMI and heart weight were significantly higher for cases without thrombosis in comparison with those with plaque rupture (p values 0.028 and 0.003, respectively). Our results indicating that increased BMI and overweight hearts are associated with chronic ischemic heart disease are compatible with clinical studies. Performing more postmortem studies on forensic autopsies, including modern radiological examinations with MPMCTA, can enhance the detection of vulnerable plaques in living patients and prevent sudden cardiac death.

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BACKGROUND AND PURPOSE: We compared among young patients with ischemic stroke the distribution of vascular risk factors among sex, age groups, and 3 distinct geographic regions in Europe. METHODS: We included patients with first-ever ischemic stroke aged 15 to 49 years from existing hospital- or population-based prospective or consecutive young stroke registries involving 15 cities in 12 countries. Geographic regions were defined as northern (Finland, Norway), central (Austria, Belgium, France, Germany, Hungary, The Netherlands, Switzerland), and southern (Greece, Italy, Turkey) Europe. Hierarchical regression models were used for comparisons. RESULTS: In the study cohort (n=3944), the 3 most frequent risk factors were current smoking (48.7%), dyslipidemia (45.8%), and hypertension (35.9%). Compared with central (n=1868; median age, 43 years) and northern (n=1330; median age, 44 years) European patients, southern Europeans (n=746; median age, 41 years) were younger. No sex difference emerged between the regions, male:female ratio being 0.7 in those aged <34 years and reaching 1.7 in those aged 45 to 49 years. After accounting for confounders, no risk-factor differences emerged at the region level. Compared with females, males were older and they more frequently had dyslipidemia or coronary heart disease, or were smokers, irrespective of region. In both sexes, prevalence of family history of stroke, dyslipidemia, smoking, hypertension, diabetes mellitus, coronary heart disease, peripheral arterial disease, and atrial fibrillation positively correlated with age across all regions. CONCLUSIONS: Primary preventive strategies for ischemic stroke in young adults-having high rate of modifiable risk factors-should be targeted according to sex and age at continental level.

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Trends in age-specific and age-standardized death certification rates from all ischaemic heart disease and cerebrovascular disease in Switzerland have been analysed for the period 1969-87, i.e. since the introduction of the Eighth Revision of the International Classification of Diseases for coding causes of death. For coronary heart disease, overall age-standardized rates of males in the mid-late 1980's were similar to those in the late 1960's, although some upward trend was evident up to the mid 1970's (with a peak rate of 120.4/100,000, World standard, in 1978) followed by steady declines in more recent years (103.8/100,000 in 1987). These falls were larger in truncated (35 to 64 years) rates. For females, overall age-standardized rates were stable around a value of 40/100,000, while truncated rates tended to decrease, particularly over most recent years, with an overall decline of over 25%. Examination of age-specific trends showed that in both sexes declines at younger ages were already evident in the earlier calendar period, while above age 50 some fall became evident only in most recent years. Thus, in a formal log-linear age/period/cohort model, both a period and a cohort component emerged. In relation to cerebrovascular diseases, the overall declines were around 40% in males (from 67.4 to 41.2/100,000, World standard) and 45% for females (from 56.6 to 31.7/100,000), and were proportionally comparable across subsequent age groups above age 45. The estimates for the age/period/cohort model were thus downwards both for the period and the cohort component although, in such a situation, it is difficult to disentangle the major underlying component.(ABSTRACT TRUNCATED AT 250 WORDS)

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Lyme disease is the most common tick-borne disease in Europe and in the United States. In comparison to dermatological, neurological and rheumatological manifestations, heart disease is quite rare. Atrioventricular heart block is nevertheless the most frequent cardiological manifestation. We hereby report the case of a patient with high degree heart block due to Lyme disease. We focus on the electrocardiographical evolution during antibiotic therapy, as well as on microbiological and diagnostic aspects. Lyme disease is a rare cause of conduction disturbances but it is treatable and potentially reversible.

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Untill recently, congenital heart disease was considered as a childhood's disease. With improvement in pediatric survival, adults with a congenital heart disease (ACHD) represent an emerging group of patients who need specialized medical care. In 2010, the ESC published newguidelines on global and specific management of adults with congenital heart disease. ACHD centers organize appropriate medical care for these patients, promote specialist training and national scientific research in collaboration with other national ACHD centers.

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Background: Low to moderate alcohol consumption has been associated with lower coronary heart disease (CHD) risk, an effect mainly mediated by an increase in HDL-cholesterol levels. However, data on the CHD risk associated with high alcohol consumption are conflicting. Methods: In a population-based study of 5,769 men and women, aged 35-75 years, without cardiovascular disease in Switzerland, last week alcohol consumption was categorized into 0, 1-6, 7-13, 14-20, 21-27, 28-34, 035 drinks/week and into nondrinkers (0 drink/week), moderate (1-13), high (14-34) and very high drinkers (035). Blood pressure, lipids and high sensitivity C-reactive protein (hs-CRP) were measured, and the 10-year CHD risk was calculated according to the Framingham risk score. Results: 73% (n = 4,214) of the participants consumed alcohol; 16% (n = 909) were considered as high drinkers and 2% (n = 119) as very high drinkers. In multivariate analysis, increasing alcohol consumption was associated with higher HDL-cholesterol (from 1.57 ± 0.01 [adjusted mean ± SE] in nondrinkers to 1.88 ± 0.03 mmol/L in very high drinkers); triglycerides (1.17 ± 1.01 to 1.32 ± 1.05 mmol/L), and systolic and diastolic blood pressure rose significantly (127.4 ± 0.4 to 132.2 ± 1.4 and 78.7 ± 0.3 to 81.7 ± 0.9 mm Hg, respectively, all p for trend <0.001). Predicted 10-year CHD risk increased from 4.31 ± 0.10 to 4.90 ± 0.37 (p = 0.03) with increasing alcohol use, with a J-shaped relationship. Conclusion: As measured by the 10-year CHD risk, the protective effect of alcohol consumption disappears in very high drinkers, namely because the beneficial increase in HDL-cholesterol may be blunt by a rise in blood pressure levels.

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Acute cardiovascular dysfunction occurs perioperatively in more than 20% of cardiosurgical patients, yet current acute heart failure (HF) classification is not applicable to this period. Indicators of major perioperative risk include unstable coronary syndromes, decompensated HF, significant arrhythmias and valvular disease. Clinical risk factors include history of heart disease, compensated HF, cerebrovascular disease, presence of diabetes mellitus, renal insufficiency and high-risk surgery. EuroSCORE reliably predicts perioperative cardiovascular alteration in patients aged less than 80 years. Preoperative B-type natriuretic peptide level is an additional risk stratification factor. Aggressively preserving heart function during cardiosurgery is a major goal. Volatile anaesthetics and levosimendan seem to be promising cardioprotective agents, but large trials are still needed to assess the best cardioprotective agent(s) and optimal protocol(s). The aim of monitoring is early detection and assessment of mechanisms of perioperative cardiovascular dysfunction. Ideally, volume status should be assessed by 'dynamic' measurement of haemodynamic parameters. Assess heart function first by echocardiography, then using a pulmonary artery catheter (especially in right heart dysfunction). If volaemia and heart function are in the normal range, cardiovascular dysfunction is very likely related to vascular dysfunction. In treating myocardial dysfunction, consider the following options, either alone or in combination: low-to-moderate doses of dobutamine and epinephrine, milrinone or levosimendan. In vasoplegia-induced hypotension, use norepinephrine to maintain adequate perfusion pressure. Exclude hypovolaemia in patients under vasopressors, through repeated volume assessments. Optimal perioperative use of inotropes/vasopressors in cardiosurgery remains controversial, and further large multinational studies are needed. Cardiosurgical perioperative classification of cardiac impairment should be based on time of occurrence (precardiotomy, failure to wean, postcardiotomy) and haemodynamic severity of the patient's condition (crash and burn, deteriorating fast, stable but inotrope dependent). In heart dysfunction with suspected coronary hypoperfusion, an intra-aortic balloon pump is highly recommended. A ventricular assist device should be considered before end organ dysfunction becomes evident. Extra-corporeal membrane oxygenation is an elegant solution as a bridge to recovery and/or decision making. This paper offers practical recommendations for management of perioperative HF in cardiosurgery based on European experts' opinion. It also emphasizes the need for large surveys and studies to assess the optimal way to manage perioperative HF in cardiac surgery.

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Background: To study the characteristics of vascular aphasia in a cohort of patients with a first-ever stroke. Methods: All patients admitted to the Lausanne neurology department for a first-ever stroke between 1979 and 2004 were included. Neurological examination including language was performed on admission. Stroke risk factors, stroke origin and location, associated symptoms and Rankin scale scores were recorded for each patient. The influence of these factors on aphasia frequency and subtypes was analyzed using logistic regression models. Results: 1,541 (26%) of patients included in this study had aphasia. The more frequent clinical presentations were expressive-receptive aphasia (38%) and mainly expressive aphasia (37%), whereas mainly receptive aphasia was less frequently observed (25%). In ischemic stroke, the frequency of aphasia increased with age (55% of nonaphasic vs. 61% of aphasic patients were more than 65 years old), female sex (40% of women in the nonaphasia group vs. 44% in the aphasia group) and risk factors for cardioembolic origin (coronary heart disease 20 vs. 26% and atrial fibrillation 15 vs. 24%). Stroke aphasia was more likely associated with superficial middle cerebral artery (MCA) stroke and leads to relevant disability. Clinical subtypes depended on stroke location and associated symptoms. Exceptions to the classic clinical-topographic correlations were not rare (26%). Finally, significant differences were found for patients with crossed aphasia in terms of stroke origin and aphasia subtypes. Conclusions: Risk factors for stroke aphasia are age, cardioembolic origin and superficial MCA stroke. Exceptions to classic clinical-topographic correlations are not rare. Stroke aphasia is associated with relevant disability. Stroke location and associated symptoms strongly influence aphasia subtypes.

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BACKGROUND: Subclinical hypothyroidism has been associated with systolic and diastolic cardiac dysfunction and an elevated cholesterol level, but data on cardiovascular outcomes and death are limited. METHODS: We studied 2730 men and women, aged 70 to 79 years, with baseline thyrotropin (TSH) measurements and 4-year follow-up data to determine whether subclinical hypothyroidism was associated with congestive heart failure (CHF), coronary heart disease, stroke, peripheral arterial disease, and cardiovascular-related and total mortality. After the exclusion of participants with abnormal thyroxine levels, subclinical hypothyroidism was defined as a TSH level of 4.5 mIU/L or greater, and was further classified according to TSH levels (4.5-6.9, 7.0-9.9, and > or = 10.0 mIU/L). RESULTS: Subclinical hypothyroidism was present in 338 (12.4%) of the participants. Compared with euthyroid participants, CHF events occurred more frequently among those with a TSH level of 7.0 mIU/L or greater (35.0 vs 16.5 per 1000 person-years; P = .006), but not among those with TSH levels between 4.5 and 6.9 mIU/L. In multivariate analyses, the risk of CHF was higher among those with high TSH levels (TSH of 7.0-9.9 mIU/L: hazard ratio, 2.58 [95% confidence interval, 1.19-5.60]; and TSH of > or = 10.0 mIU/L: hazard ratio, 3.26 [95% confidence interval, 1.37-7.77]). Among the 2555 participants without CHF at baseline, the hazard ratio for incident CHF events was 2.33 (95% confidence interval, 1.10-4.96; P = .03) in those with a TSH of 7.0 mIU/L or greater. Subclinical hypothyroidism was not associated with increased risk for coronary heart disease, stroke, peripheral arterial disease, or cardiovascular-related or total mortality. CONCLUSIONS: Subclinical hypothyroidism is associated with an increased risk of CHF among older adults with a TSH level of 7.0 mIU/L or greater, but not with other cardiovascular events and mortality. Further investigation is warranted to assess whether subclinical hypothyroidism causes or worsens preexisting heart failure.

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OBJECTIVES: This study sought to establish an accurate and reproducible T(2)-mapping cardiac magnetic resonance (CMR) methodology at 3 T and to evaluate it in healthy volunteers and patients with myocardial infarct. BACKGROUND: Myocardial edema affects the T(2) relaxation time on CMR. Therefore, T(2)-mapping has been established to characterize edema at 1.5 T. A 3 T implementation designed for longitudinal studies and aimed at guiding and monitoring therapy remains to be implemented, thoroughly characterized, and evaluated in vivo. METHODS: A free-breathing navigator-gated radial CMR pulse sequence with an adiabatic T(2) preparation module and an empirical fitting equation for T(2) quantification was optimized using numerical simulations and was validated at 3 T in a phantom study. Its reproducibility for myocardial T(2) quantification was then ascertained in healthy volunteers and improved using an external reference phantom with known T(2). In a small cohort of patients with established myocardial infarction, the local T(2) value and extent of the edematous region were determined and compared with conventional T(2)-weighted CMR and x-ray coronary angiography, where available. RESULTS: The numerical simulations and phantom study demonstrated that the empirical fitting equation is significantly more accurate for T(2) quantification than that for the more conventional exponential decay. The volunteer study consistently demonstrated a reproducibility error as low as 2 ± 1% using the external reference phantom and an average myocardial T(2) of 38.5 ± 4.5 ms. Intraobserver and interobserver variability in the volunteers were -0.04 ± 0.89 ms (p = 0.86) and -0.23 ± 0.91 ms (p = 0.87), respectively. In the infarction patients, the T(2) in edema was 62.4 ± 9.2 ms and was consistent with the x-ray angiographic findings. Simultaneously, the extent of the edematous region by T(2)-mapping correlated well with that from the T(2)-weighted images (r = 0.91). CONCLUSIONS: The new, well-characterized 3 T methodology enables robust and accurate cardiac T(2)-mapping at 3 T with high spatial resolution, while the addition of a reference phantom improves reproducibility. This technique may be well suited for longitudinal studies in patients with suspected or established heart disease.

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IMPORTANCE: The 2013 American College of Cardiology/American Heart Association (ACC/AHA) guidelines introduced a prediction model and lowered the threshold for treatment with statins to a 7.5% 10-year hard atherosclerotic cardiovascular disease (ASCVD) risk. Implications of the new guideline's threshold and model have not been addressed in non-US populations or compared with previous guidelines. OBJECTIVE: To determine population-wide implications of the ACC/AHA, the Adult Treatment Panel III (ATP-III), and the European Society of Cardiology (ESC) guidelines using a cohort of Dutch individuals aged 55 years or older. DESIGN, SETTING, AND PARTICIPANTS: We included 4854 Rotterdam Study participants recruited in 1997-2001. We calculated 10-year risks for "hard" ASCVD events (including fatal and nonfatal coronary heart disease [CHD] and stroke) (ACC/AHA), hard CHD events (fatal and nonfatal myocardial infarction, CHD mortality) (ATP-III), and atherosclerotic CVD mortality (ESC). MAIN OUTCOMES AND MEASURES: Events were assessed until January 1, 2012. Per guideline, we calculated proportions of individuals for whom statins would be recommended and determined calibration and discrimination of risk models. RESULTS: The mean age was 65.5 (SD, 5.2) years. Statins would be recommended for 96.4% (95% CI, 95.4%-97.1%; n = 1825) of men and 65.8% (95% CI, 63.8%-67.7%; n = 1523) of women by the ACC/AHA, 52.0% (95% CI, 49.8%-54.3%; n = 985) of men and 35.5% (95% CI, 33.5%-37.5%; n = 821) of women by the ATP-III, and 66.1% (95% CI, 64.0%-68.3%; n = 1253) of men and 39.1% (95% CI, 37.1%-41.2%; n = 906) of women by ESC guidelines. With the ACC/AHA model, average predicted risk vs observed cumulative incidence of hard ASCVD events was 21.5% (95% CI, 20.9%-22.1%) vs 12.7% (95% CI, 11.1%-14.5%) for men (192 events) and 11.6% (95% CI, 11.2%-12.0%) vs 7.9% (95% CI, 6.7%-9.2%) for women (151 events). Similar overestimation occurred with the ATP-III model (98 events in men and 62 events in women) and ESC model (50 events in men and 37 events in women). The C statistic was 0.67 (95% CI, 0.63-0.71) in men and 0.68 (95% CI, 0.64-0.73) in women for hard ASCVD (ACC/AHA), 0.67 (95% CI, 0.62-0.72) in men and 0.69 (95% CI, 0.63-0.75) in women for hard CHD (ATP-III), and 0.76 (95% CI, 0.70-0.82) in men and 0.77 (95% CI, 0.71-0.83) in women for CVD mortality (ESC). CONCLUSIONS AND RELEVANCE: In this European population aged 55 years or older, proportions of individuals eligible for statins differed substantially among the guidelines. The ACC/AHA guideline would recommend statins for nearly all men and two-thirds of women, proportions exceeding those with the ATP-III or ESC guidelines. All 3 risk models provided poor calibration and moderate to good discrimination. Improving risk predictions and setting appropriate population-wide thresholds are necessary to facilitate better clinical decision making.

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Background: Inflammation is associated with heart failure (HF) risk factors and also directly affects myocardial function. However, the association between inflammation and HF risk in older adults has not been adequately evaluated. Methods: The association of baseline serum concentrations of interleukin-6 (IL-6), tumor necrosis factor alpha (TNF- ), and C-reactive protein (CRP) with incident HF was assessed with Cox proportional hazards models among 2610 older persons without prevalent HF enrolled in the Health, Aging, and Body Composition (Health ABC) Study (age, 73.6±2.9 years; 48.3% men; 59.6% white). Results: Median (interquartile range) baseline concentrations of IL-6, TNF- , and CRP were 1.80 (1.23, 2.76) pg/mL, 3.14 (2.41, 4.06) pg/mL, and 1.64 (0.99, 3.04) µg/mL, respectively. On follow-up (median, 9.4 years), 311 participants (11.9%) developed HF. In models controlling for clinical predictors of HF and incident coronary heart disease, doubling of IL-6, TNF- , and CRP concentrations was associated with 34% (95% CI, 18 -52%; P<.001), 33% (95% CI, 9 - 63%; P=.006), and 13% (95% CI, 3-24%; P=.01) increase in HF risk, respectively. In models including all 3 markers, IL-6 and TNF- , but not CRP, remained significant. Findings were similar across sex and race. Post-HF ejection fraction (EF) was available in 239 (76.8%) cases. When only cases with preserved EF were considered (n=105), IL-6 (HR per doubling, 1.57; 95% CI, 1.28 -1.94; P<.001), TNF- (HR per doubling, 1.59; 95% CI, 1.12-2.26; P=.01), and CRP (HR per doubling, 1.23; 95% CI, 1.05-1.44; P=.01) were all associated with HF risk in adjusted models. In contrast, when only cases with reduced EF (n=134) were considered, only IL-6 attained marginal significance in adjusted models (HR per doubling, 1.20; 95% CI, 0.99 -1.46; P=.06). Participants with 2 or 3 markers above median had pronounced HF risk in adjusted models (HR, 1.66; 95% CI, 1.12-2.46; P=.01; and HR, 1.76; 95% CI, 1.16 -2.65; P=.007, respectively). Addition of IL-6 to the clinical Health ABC HF model improved discrimination (C index from 0.717 to 0.734; P=.001) and fit (decreased Bayes information criterion by 17.8; P<.001). Conclusions: Inflammatory markers are associated with HF risk among older adults and may improve HF risk stratification.