Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been shown that certain patients with cirrhosis have asymptomatic cardiac abnormalities that have not yet been explained. Thus, cardiac troponin I, a specific marker of myocardial injury, has been measured in patients with cirrhosis without previous cardiac disease. Thirty-two consecutive patients (age 49 +/- 11) with cirrhosis and normal ECG were selected, 22 of which were alcoholic. Hemodynamic investigations were performed. Left ventricular function and mass were evaluated by echocardiography. Serum creatine kinase MB mass, myoglobin, and cardiac troponin I concentrations were measured. Cardiac troponin I concentrations were elevated in 10 patients (32%) (range 0.06-0.25 microg/L) whereas creatine kinase MB mass and myoglobin were normal in all patients. Abnormal troponin I values were not related to the severity of cirrhosis, to the degree of portal hypertension, or to other hemodynamic values. In contrast, elevated serum cardiac troponin I concentrations were related to a decreased stroke-volume index (P <. 05) and a decreased left ventricular mass (P <.05). These results show a high prevalence of slightly elevated serum cardiac troponin I in patients with cirrhosis, especially in those with alcoholic cirrhosis. Elevated troponin I is associated with subclinical left ventricular myocardial damage. These findings may be linked to a lack of left ventricular adaptation in certain patients with cirrhosis and alcoholic cardiomyopathy.
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PMID:Elevated circulating cardiac troponin I in patients with cirrhosis. 1005 61

We investigated the use of measurements of serum concentrations of the cardiac proteins troponins I and T as biochemical markers of myocardial cell damage in 80 patients undergoing vascular or major orthopaedic surgery. Holter electrocardiographic monitoring was carried out before surgery and for 3 days after surgery. Blood samples for troponins I and T and creatine kinase-MB isoenzyme were taken on each of these 4 days. Outcome was assessed at 3 months using a patient questionnaire, general practitioner follow-up and case notes review. Silent postoperative myocardial ischaemia was detected in 21 patients; increases in troponins I and T and creatine kinase-MB occurred in four, six and 17 of these patients, respectively. Eight patients suffered major postoperative complications (cardiac death, myocardial ischaemia, congestive cardiac failure, unstable angina and cerebrovascular accident) and 21 minor complications (poorly controlled hypertension needing increased or new additional treatment, palpitations, increased tiredness or shortness of breath in the absence of known respiratory disease). There were no associations between postoperative ischaemia and cardiac protein concentrations. The relative odds for the associations of major adverse outcome at 3 months after surgery and postoperative ischaemia or increased serum concentrations of the three proteins were 5.39 [95% confidence intervals 1.16-27.67] for postoperative ischaemia; 5.64 [1.07-31.00] for creatine kinase-MB isoenzyme; 17.00 [2.20-116.54] for troponin T and 13.20 [1.12-135.00] for troponin I. We found troponin T to be the only prospective marker for both major and minor cardiovascular complications (relative odds 10.65 [1.26-252.88]).
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PMID:Increases in serum concentrations of cardiac proteins and the prediction of early postoperative cardiovascular complications in noncardiac surgery patients. 1155 Jun 85

The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin)-mediated lowering of serum cholesterol has been associated with a significant reduction in cardiovascular morbidity and mortality. Recent studies suggest that additional non-lipid lowering effects (eg, endothelial stabilization, anti-inflammatory, antithrombogenic) may be important in modulating their effectiveness. Dyslipidemia is common in end-stage renal disease (ESRD), and hemodialysis patients have increased cardiovascular morbidity and mortality. Cerivastatin, a new statin with powerful low-density lipoprotein-cholesterol (LDL-C) lowering capabilities, possesses some unique non-LDL-C-mediated properties that may contribute to a reduction of coronary events in the patient with ESRD. The primary objective of this multicenter multinational study of 1,054 hemodialysis patients is to compare 2 years of treatment with cerivastatin (0.4 mg/d) versus placebo on the composite clinical event rate of myocardial infarction, sudden cardiac death, ischemic stroke, and the need for coronary arterial bypass graft (CABG) or percutaneous transluminal coronary angioplasty (PTCA) procedures in these patients. Changes in lipids, inflammatory proteins including heat stable C-reactive protein (hsCRP), interleukin-6 (IL-6), oncostatin-M, intracellular adhesion molecule-1 (ICAM-1) and monocyte-chemoattractant protein-1 (MCP-1), as well as markers of cardiac muscle pathology, such as troponin I and troponin T, will be assessed in a subset of patients. This study is the first of its kind to assess the effect of a statin on the reduction of cardiovascular morbidity and mortality in an incident hemodialysis population. It will determine whether treatment with cerivastatin can effectively reduce the significant cardiovascular morbidity and mortality.
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PMID:The CHORUS (Cerivastatin in Heart Outcomes in Renal Disease: Understanding Survival) protocol: a double-blind, placebo-controlled trial in patients with esrd. 1115 61

In cardiovascular pharmacotherapy, the main focus is now on statins (HMG-CoA-reductase inhibitors) because of their antihyperlipidaemic and antiatherogenic effect. They are suggested to be beneficial also in senile dementia, stroke and osteoporosis and they can reduce incidence of ventricular arrhythmias in patients with cardioverter-defibrillator. In chronic heart failure, statins should be used with caution since reduced cholesterol levels relate to impaired survival. As an alternative to statins and fibrates, niacin therapy may be considered. ACE inhibitors are of proven benefit for patients with left ventricular dysfunction after acute myocardial infarction; however, in long-term treatment, their protective activity is not superior to that of beta-blockers, diuretics and clonidine. Ca-channel antagonists slightly increase the incidence of cardiovascular complications but reduce the incidence of stroke in high-risk patients. Biventricular pacing has been used with success in patients with severe heart failure and conduction disturbances, and the first permanent artificial ventricle was implanted to a patient with irreversible terminal heart failure in summer 2000. Cardiospecific troponin I may be an uninvasive marker of a procoagulant status indicating e.g. graft failure after cardiac transplantation; T-cadherin belongs to the cell-adhesion molecules and has a role in maintenance of cellular contacts which are critical for the vessel wall architecture. Etamoxir, originally developed for the treatment of diabetes II, has recently been shown to be a potential novel drug for heart failure. Routine use of nitric oxide after congenital heart surgery lessens the risk of pulmonary hypertensive crises.
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PMID:[Cardiology 2000]. 1137 23

beta-Adrenergic stimulation increases stroke volume in mammalian hearts as a result of protein kinase A (PKA)-induced phosphorylation of several myocyte proteins. This study investigated whether PKA-induced phosphorylation of myofibrillar proteins directly affects myocyte contractility. To test this possibility, we compared isometric force, loaded shortening velocity, and power output in skinned rat cardiac myocytes before and after treatment with the catalytic subunit of PKA. Consistent with previous studies, PKA increased phosphorylation levels of myosin binding protein C and troponin I, and reduced Ca(2+) sensitivity of force. PKA also significantly increased both maximal force (25.4+/-8.3 versus 31.6+/-11.3 microN [P<0.001, n=12]) and peak absolute power output (2.48+/-1.33 versus 3.38+/-1.52 microW/mg [P<0.05, n=5]) during maximal Ca(2+) activations. Furthermore, PKA elevated power output at nearly all loads even after normalizing for the increase in force. After PKA treatment, peak normalized power output increased approximately 20% during maximal Ca(2+) activations (n=5) and approximately 33% during half-maximal Ca(2+) activations (n=9). These results indicate that PKA-induced phosphorylation of myofibrillar proteins increases the power output-generating capacity of skinned cardiac myocytes, in part, by speeding the step(s) in the crossbridge cycle that limit loaded shortening rates, and these changes likely contribute to greater contractility in hearts after beta-adrenergic stimulation.
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PMID:Power output is increased after phosphorylation of myofibrillar proteins in rat skinned cardiac myocytes. 1173 84

Patients with acute cerebrovascular diseases may present a great variety of electrocardiographic abnormalities. Electrocardiographic pattern consistent with acute myocardial infarction (AMI) without biochemical evidence of myocardial necrosis associated with ischemic stroke is exceptional. It is described a 86-year-old woman with an electrocardiographic pattern consistent with AMI, with normal creatinkinase and troponin I levels, associated with a right hemispheric ischemic stroke.
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PMID:[Electrocardiographic abnormalities consistent with acute myocardial infarction associated with ischemic stroke]. 1248 61

Cardiac troponin C is the Ca2+-dependent switch for heart muscle contraction. Troponin C is associated with various other proteins including troponin I and troponin T. The interaction between the subunits within the troponin complex is of critical importance in understanding contractility. Following a Ca2+ signal to begin contraction, the inhibitory region of troponin I comprising residues Thr128-Arg147 relocates from its binding surface on actin to troponin C, triggering movement of troponin-tropomyosin within the thin filament and thereby freeing actin-binding site(s) for interactions with the myosin ATPase of the thick filament to generate the power stroke. The structure of calcium-saturated cardiac troponin C (C-domain) in complex with the inhibitory region of troponin I was determined using multinuclear and multidimensional nuclear magnetic resonance spectroscopy. The structure of this complex reveals that the inhibitory region adopts a helical conformation spanning residues Leu134-Lys139, with a novel orientation between the E- and H-helices of troponin C, which is largely stabilized by electrostatic interactions. By using isotope labeling, we have studied the dynamics of the protein and peptide in the binary complex. The structure of this inhibited complex provides a framework for understanding into interactions within the troponin complex upon heart contraction.
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PMID:Structure and dynamics of the C-domain of human cardiac troponin C in complex with the inhibitory region of human cardiac troponin I. 1273 41

We have previously demonstrated that the peri-operative measurement of increased serum concentrations of the cardiac markers troponins I and T and creatine kinase-MB can be predictors of major cardiovascular outcomes (including cardiac death) at 3 months after surgery. In the present study, we have followed the postoperative course of 157 patients undergoing major vascular surgery or major joint arthroplasty to 1 year using a patient questionnaire, general practitioner follow-up and case-notes review. Increased postoperative marker concentrations were defined as values greater than the upper reference limit. Increases in troponin I and troponin T concentrations, as well as a single elevated creatine kinase-MB and two successively elevated creatine kinase-MB concentrations were measured in 12, 13, 33 and 15 patients respectively. Thirty-nine major adverse cardiac outcomes were recorded (cardiac death, myocardial ischaemia, congestive cardiac failure, unstable angina, cerebrovascular accident and major arrhythmias needing active treatment). There was no association between increases in any of these cardiac markers and cardiac death to 1 year. However, increases in troponin I and both a single elevated creatine kinase-MB and two successively elevated creatine kinase-MB concentrations were associated with an increased incidence of major cardiac outcomes, including cardiac death, to 1 year (odds ratio [95% confidence intervals] = 4.19 [1.16-14.87], 3.97 [1.65-9.44] and 5.19 [1.60-16.22], respectively).
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PMID:Peri-operative troponin I concentration as a marker of long-term postoperative adverse cardiac outcomes--a study in high-risk surgical patients. 1502

Although several clinical studies have shown that increased serum concentrations of protein S100B predict ischaemic brain damage after cardiac surgery, S100B may also be released from the heart or other injured tissue. We therefore investigated the correlation between serum S100B levels and those of the specific cardiac marker troponin I in order to assess the cerebral vs. extracerebral origin of S100B. In 64 cardiac surgical patients, serial blood samples were drawn for the measurement of S100B and troponin I before surgery and for seven days after surgery. Neurological function was assessed before with the National Institutes of Health Stroke Scale and the Folstein Mini Mental Test. The data show that a sustained increase in serum S100B levels is associated with neurological dysfunction, as witnessed by a positive correlation between S100B values and the results of the neuropsychological tests. In contrast, the early postoperative increased levels of protein S100B derive from cardiac tissue, as shown by the positive correlation between S100B and cardiac troponin I levels.
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PMID:Cerebral and extracerebral release of protein S100B in cardiac surgical patients. 1547 42

Beneficial actions of nitric oxide (NO) in failing myocardium have frequently been overshadowed by poorly documented negative inotropic effects mainly derived from in vitro cardiac preparations. NO's beneficial actions include control of myocardial energetics and improvement of left ventricular (LV) diastolic distensibility. In isolated cardiomyocytes, administration of NO increases their diastolic cell length consistent with a rightward shift of the passive length-tension relation. This shift is explained by cGMP-induced phosphorylation of troponin I, which prevents calcium-independent diastolic cross-bridge cycling and concomitant diastolic stiffening of the myocardium. Similar improvements in diastolic stiffness have been observed in isolated guinea pig hearts, in pacing-induced heart failure dogs, and in patients with dilated cardiomyopathy or aortic stenosis and have been shown to result in higher LV preload reserve and stroke work. NO also controls myocardial energetics through its effects on mitochondrial respiration, oxygen consumption, and substrate utilization. The effects of NO on diastolic LV performance appear to be synergistic with its effects on myocardial energetics through prevention of myocardial energy wastage induced by LV contraction against late-systolic reflected arterial pressure waves and through prevention of diastolic LV stiffening, which is essential for the maintenance of adequate subendocardial coronary perfusion. A drop in these concerted actions of NO on diastolic LV distensibility and on myocardial energetics could well be instrumental for the relentless deterioration of failing myocardium.
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PMID:Nitric oxide's role in the heart: control of beating or breathing? 1521 Apr 49


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