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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifty patients with acute myocardial infarction were studied serially to evaluate the extent and nature of functional cardiovascular impairment and the time course of recovery. Reinfarction or death occurred in six patients. Peak workload during bicycle exercise in a subgroup of 25 patients with maximal initial test and complete follow-up increased from 334 to 409 kpm/min (P less than 0.01) bwtween three and six weeks. There was further significant (P less than 0.01) improvement between three and six months from 438 to 488 kpm/min. The incidence of ischemia at a constant workload decreased between three and six weeks without any significant changes in heart rate or blood pressure. Mean cardiac output during exercise at three months was 6.5 and at six months 7.8 L/min (P less than 0.05). Corresponding values for stroke volume were 61 and 72 ml (P less than 0.05). The data suggest that in clinically stable patients there is an early improvement of the relation between myocardial oxygen supply and demand and a late improvement of functional capacity associated with increased stroke volume and cardiac output.
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PMID:Cardiovascular function during early recovery from acute myocardial infarction. 92 62

Sixteen patients with progressive systemic sclerosis (PSS), including 3 with the "CREST" (calcinosis, Raynaud's, esophageal dysfunction, sclerodactyly, and/or telangiectasias) variant, were evaluated with resting M-mode echocardiography and noninvasive measurements of cardiac output at rest and during submaximal exercise to determine the nature and extent of any cardiovascular impairment. No patient had arterial hypertension, significant renal impairment, clinical evidence of large vessel coronary artery disease, or severe pulmonary dysfunction. The duration of disease was 1 to 12 years (9 to 30 for patients with the CREST variant). Echocardiographic abnormalities included increased right ventricular dimension (3 patients), reduced left ventricular ejection fraction (3 patients), and pericardial effusion (3 patients). Cardiac index (CI) and stroke volume index (SVI) at rest were similar for patients and controls. Patients and controls were exercised to similar heart rates (130 +/- 3 vs 124 +/- 4; p, NS). Total peripheral resistance (TPR) was higher for patients (1123 +/- 81 vs 810 +/- 44 dyn X s X cm-5) and their mean SVI failed to increase significantly compared with sitting rest values (30 +/- 2 vs 35 +/- 3 ml/m2). The control subjects had the expected increase in SVI (36 +/- 2 vs 51 +/- 5; p less than 0.01). Ten patients with an abnormal hemodynamic response to exercise had a normal echocardiographic circumferential fiber shortening (VCF) or ejection fraction (EF) at rest. The data indicate that PSS patients have a greater degree of cardiovascular dysfunction than would be predicted from clinical data and laboratory evaluation of cardiovascular and pulmonary function at rest. Multiple mechanisms, including right and left ventricular dysfunction and abnormal vasoconstrictor activity, are likely to contribute to the reduction in exercise capacity seen in patients with PSS.
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PMID:Cardiovascular function in patients with progressive systemic sclerosis (scleroderma). 621 13

Forty-four patients suffering a stroke for the first time were examined within 10 h of the onset of symptoms; the tests performed on their admission to hospital, and thereafter on the third and seventh day, were 24-h Holter EKG with spectral analysis of heart rate variability, evaluation of arterial blood pressure and the levels of catecholamine in the blood and 24-h urine. The dynamic EKG on admission revealed that 31 (70.5%) out of the 44 patients already had arrhythmia. These alterations were observed in 9 (75%) out of 12 haemorrhagic patients with a significant (P < 0.05) prevalence compared to 22 (68.8%) of the 32 ischaemic ones. Arrhythmia showed up in 16 (76.2%) out of 21 cases with right hemisphere lesions and in 12 (63.2%) out of 19 cases of left hemisphere lesions; this difference was also significant (P<0.05). Arrhythmia was still present in 19 (43.2%) patients after 3 days and only in 2 (6.5%) patients after 7 days. The spectral analysis parameters on admission and after 3 days were significantly (P < 0.05) modified in patients with stroke plus arrhythmia, compared to patients with stroke alone and to control subjects, whereas no further differences were observed on the seventh day. Moreover, the percentage of patients with arterial hypertension and high levels of catecholamine greatly decreased from the third day onwards. A transient autonomic nervous system imbalance with prevalent sympathetic activity may justify this cardiovascular impairment during the hyperacute phase of stroke.
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PMID:Transient autonomic nervous system dysfunction during hyperacute stroke. 1108 9

Although psoriasis is predominantly a chronic inflammatory skin disorder, it has been known to be associated with cardiovascular disease. Patients with psoriasis, particularly with moderate to severe forms, present an increased rate of cardiovascular mortality, myocardial infarction and stroke. However the pathophysiology of the relationship between psoriasis and cardiovascular risk and comorbidities has not yet completely known. Chronic inflammation may be considered a solid link between psoriasis and related cardiovascular events. Several cytokines and inflammatory cells play a pivotal role in the development of psoriatic lesions, resulting in angiogenesis and endothelial dysfunction. Furthermore, the imbalance between oxidative stress and antioxidant mechanisms in psoriatic patients may contribute to explain the pathogenesis of increased reactive oxygen species and the formation of atherosclerotic plaque. Other mechanistic pathways which may be involved in this relationship include cardiovascular effects of medications, a common genetic background and a higher prevalence of cardiovascular risk factors, which are often under-diagnosed and under-treated in psoriatic patients. Indeed, the early detection of specific markers of cardiovascular impairment, such as N-terminal pro B-type natriuretic peptide, homocysteine and YKL-40, may enable psoriatic patients at higher cardiovascular risk to be identified as soon as possible. This review examines the increased cardiovascular risk profile and high prevalence of cardiovascular disease associated with psoriasis, focusing on pathogenic links between psoriasis and atherosclerosis, serological markers of cardiovascular involvement and the implications of antipsoriatic therapies on cardiovascular risk and proposes a flow chart, that every dermatologist should follow to screen psoriatic patients.
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PMID:Psoriasis as a cardiovascular risk factor: updates and algorithmic approach. 2968 93

The microbiota-gut-brain axis is considered a central regulator of the immune system after acute ischemic stroke (AIS), with a potential role in determining outcome. Several pathways are involved in the evolution of gut microbiota dysbiosis after AIS. Brain-gut and gut-brain signaling pathways involve bidirectional communication between the hypothalamic-pituitary-adrenal axis, the autonomic nervous system, the enteric nervous system, and the immune cells of the gut. Alterations in gut microbiome can be a risk factor and may also lead to AIS. Both risk factors for AIS and gut-microbiome composition are influenced by similar factors, including diabetes, hypertension, hyperlipidemia, obesity, and vascular dysfunction. Furthermore, the systemic inflammatory response after AIS may yield liver, renal, respiratory, gastrointestinal, and cardiovascular impairment, including the multiple organ dysfunction syndrome. This review focus on biochemical, immunological, and neuroanatomical modulation of gut microbiota and its possible systemic harmful effects after AIS, as well as the role of ischemic stroke on microbiota composition. Finally, we highlight the role of gut microbiota as a potential novel therapeutic target in acute ischemic stroke.
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PMID:Gut Microbiota in Acute Ischemic Stroke: From Pathophysiology to Therapeutic Implications. 3267 Jan 91