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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We evaluated whether recent cocaine use alters the specificity of CK-MB, myoglobin, and cardiac troponin I for acute myocardial infarction (AMI) in patients who are seen in the emergency department for chest pain. Patients <60 years old with potential myocardial ischemia underwent a standardized history and physical examination and routine CK-MB assays every 8 to 12 hours and had study serum obtained at presentation for CK-MB, myoglobin, and cardiac troponin I immunoassays, as well as benzoylecgonine, cocaine's main metabolite. We enrolled 97 patients, 19 (20%) of whom had recent used cocaine. Patients with and without cocaine use were similar with regards to sex, race, renal and muscular disease, diabetes, family history, and hypertension and rate of AMI (12% vs 11%, p = 1.0). In patients without MI, the mean myoglobin level was higher in cocaine users than noncocaine users (179 vs 74 ng/ml; Mann-Whitney p = 0.003), but the mean values were similar for CK-MB (2.2 vs 2.1 ng/ml; Mann-Whitney p = 0.58) and for cardiac troponin-I (0.02 vs 0.02 ng/ml; Mann-Whitney p = 0.87). The specificities of the markers in patients with and without cocaine use were as follows: cardiac troponin I, 94% vs 94%, (p = 1.0); CK-MB, 75% vs 88% (p = 0.24); and myoglobin, 50% vs 82%, (p = 0.02), respectively. Our data demonstrate that the specificity of myoglobin was altered by recent cocaine use. The specificity of CK-MB was affected less and the specificity of cardiac troponin I was not affected by recent cocaine use.
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PMID:Effect of recent cocaine use on the specificity of cardiac markers for diagnosis of acute myocardial infarction. 948 72

Risk stratification is a key element of clinical management not only in the primary and secondary prevention, but also during the acute stages of cardiovascular disease. The current risk assessment algorithms in primary prevention are based on established risk factors: gender and age, cigarette smoking, the presence of hypertension and diabetes mellitus, and serum concentrations of total cholesterol, low-density lipoprotein (LDL)-cholesterol and high-density lipoprotein-cholesterol. However, many individuals who are assessed as "low risk" on the basis of traditional risk factors, still develop cardiac events. This article addresses current issues relevant to the assessment of cardiovascular risk. It emphasizes the potential importance of disturbed energy supply for atherogenesis, by introducing the concept of fuel transport (chylomicron, VLDL, and remnants) and overflow (LDL) pathways of lipid metabolism. It highlights the present lack of routine methods to monitor the fuel transport pathway. It considers the measurements of serum C-reactive protein and plasma fibrinogen as new additions to the cardiovascular risk factor profiles. Finally, risk stratification based on the traditional and the new risk factors is linked to that based on the markers of acute myocardial damage such as cardiac troponin I or troponin T. It is concluded that the combined use of the markers of myocardial damage and the "new" cardiovascular risk factors is the way ahead for the assessment of cardiovascular risk.
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PMID:Risk factors for coronary disease: the time for a paradigm shift? 1175 3

Electrocardiographic abnormalities, particularly in those waveforms representing ventricular repolarization, have been reported in subarachnoid hemorrhage. This study reports abnormalities on the initial electrocardiogram in 100 patients with SAH. Overall, one or more repolarization abnormalities occurred in 41% of patients. Analysis revealed prolonged QTc interval >460 ms in 16%, ST segment elevation in 9%, ST depression in 3%, T wave inversion in 7%, and U wave >or=100 microV in 15%. Electrocardiographic criteria for left ventricular hypertrophy were met in 14%, and 43% of those patients had no history of hypertension. Serum cardiac troponin I was elevated in 21%, and was significantly associated with QTc interval >460 ms (P <.001). Controlling for gender, those with QTc interval >460 ms were 5.5 times more likely to have elevated serum cardiac troponin I. It is concluded that repolarization abnormalities are present in a high proportion of patients with SAH. Some SAH patients also have left ventricular hypertrophy voltage unrelated to hypertension or coronary artery disease. Prolonged QTc interval after SAH is significantly related to myocardial injury, but unrelated to mortality, and there is no association between ST-T wave abnormalities and either myocardial injury or mortality.
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PMID:Electrocardiographic repolarization abnormalities in subarachnoid hemorrhage. 1253 36

OBJECTIVE: To investigate the correlation between RFCA catheter cumulative energy and autonomic nerve injury. METHODS: Forty-one patients with paroxysmal supraventricular tachycardia were enrolled, Patients were excluded if they had Diabetes, Hypertension, Congestive Heart Failure or other organic heart disease. HRV and biochemical markers were measured before and after the RFCA. RESULTS: Compared with pre-ablation values,there was significantly decrease in post-ablation low frequency (LF) and high frequency (HF). This was noted in both the septal group (AVNRT and septal pathway) and free wall group (free wall accessory pathway).Post-procedure,the sensitivity of cardiac troponin I(cTnI) for myocardial injury detection was 58.3%, AST was 41.7%. This was significantly higher than other markers(CK:4.2%, CK-MB:10.4%, LDH:20.8%). The post-ablation sensitivity of cTnI was 54.2%, 6.3% and 52.1%at 1 hour, 12 hours, and 24 hours respectively. A significant correlation between cumulative energy and delta HF(r=0.688,P=0.01) or delta LF (r=0.462, P<0.05).was noted in free wall group.(delta HF=pre-ablation HF-post-ablation HF/pre-ablation HF x 100%). There was no significant correlation between biochemical markers and either delta HF or delta LF. CONCLUSION: RFCA induced injury on cardiac autonomic nerves related to both cumulative energy and ablation site,but not size of myocardial injury as determined by cTnI measurement. cTnI is an excellent biochemical marker of myocardial injury.
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PMID:[Radiofrequency catheter ablation autonomic nerve injury] 1259 13

We investigated the efficacy and safety of extended enoxaparin monotherapy in symptomatic patients with acute pulmonary embolism (PE). We randomized 40 patients in a 1:1 allocation to enoxaparin monotherapy (1 mg/kg twice daily for 10-18 days, and then 1.5mg/kg once daily until day 90) (n = 20) or to enoxaparin 1.0 mg/kg twice daily as a bridge to warfarin with a target international normalized ratio of 2.0-3.0 for 90 days (at least 10 doses of enoxaparin overlapping with warfarin for at least 4 days) (n = 20). All patients underwent echocardiography, cardiac troponin I (TnI), and brain natriuretic peptide testing to identify patients with an increased likelihood of adverse clinical outcomes. The end-points were newly diagnosed deep venous thrombosis (DVT) or PE and bleeding events through day 90. In 15 patients on extended enoxaparin therapy, we used repeated measure analysis of variance (ANOVA) to investigate differences in anti-Xa levels obtained at 2, 4, 8 and 12 weeks. The patients' mean age was 52 +/- 17 years; the most common comorbidities were obesity (58%), hypertension (30%), concomitant DVT (30%) and cancer (15%). Twelve (30%) patients had elevated cardiac Tnl >0.1 mg/l and 11 (28%) had moderate or severe right ventricular dysfunction on echocardiography. Ten (25%) patients received thrombolysis with a continuous infusion of 100 mg alteplase prior to randomization. During a 90-day follow-up, one patient from the enoxaparin monotherapy group suffered symptomatic distal DVT; one from the warfarin group had recurrent symptomatic PE (p = 1.0). None of the study patients had major hemorrhage; two warfarin group patients had minor bleeding compared with none in the enoxaparin monotherapy group (p = 0.49). Repeated measure ANOVA did not reveal significant differences in anti-Xa levels over time (p = 0.217). In patients with acute symptomatic PE, extended enoxaparin monotherapy is feasible and warrants further investigation in a large clinical trial.
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PMID:Extended enoxaparin monotherapy for acute symptomatic pulmonary embolism. 1644 53

The causes of postoperative cardiovascular disturbances in neurosurgical patients include direct cardiac neurogenic effects, clinical situations where brain tissue is underperfused, and hyperdynamic states. EKG and echographic abnormalities are common in subarachnoid hemorrhage where cardiac troponin I is the most useful predictor of cardiac risk after SAH. Neurogenic pulmonary edema is short lived and often resolves with resolution of the neurologic problem. In traumatic brain injury, where areas of ischemia co-exist with luxury perfusion, advanced hemodynamic monitoring and prevention of jugular venous desaturation best avoid secondary brain injury and achieve optimal neurologic outcome. Induced hypertension improves blood flow through vessels compromised by cerebral stenting, angioplasty, microcatheters, thrombolysis, carotid clamping, intracranial bypass and cerebral vasospasm. Hyperdynamic lesions include vascular breakthrough after elimination of cerebral arteriovenous malformations, but also emergence hypertension and hyperemia. Pharmacologic agents and adjunctive measures are effective in controlling both the systemic and the cerebral circulation.
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PMID:Cardiovascular therapy of neurosurgical patients. 1828 33

The transient receptor potential vanilloid (TRPV1) channels expressed in sensory afferent fibers innervating the heart may be activated by protons or endovanilloids released during myocardial ischemia (MI), leading to angina. Although our previous in vitro data indicate that TRPV1 activation may preserve cardiac function after ischemia-reperfusion injury, the underlying mechanisms are largely unknown. To test the hypothesis that TRPV1 modulates inflammatory and early remodeling processes to prevent cardiac functional deterioration after myocardial infarction, TRPV1-null mutant (TRPV1(-/-)) and wild-type (WT) mice were subjected to left anterior descending coronary ligation or sham operation. The infarct size was greater in TRPV1(-/-) than in WT mice (P<0.001) 3 days after MI, and the mortality rate was higher in TRPV1(-/-) than in WT mice (P<0.05) 7 days after MI. The levels of plasma cardiac troponin I; cytokines, including tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6; chemokines, including monocyte chemoattractant protein-1 and macrophage inflammatory protein-2; and infiltration of inflammatory cells, including neutrophils, macrophages, and myofibroblasts; as well as collagen contents, were greater in TRPV1(-/-) than in WT mice (P<0.05) in the infarct area on days 3 and 7 after MI. Changes in left ventricular geometry led to increased end-systolic and -diastolic diameters and reduced contractile function in TRPV1(-/-) compared with WT mice. These data show that TRPV1 gene deletion results in excessive inflammation, disproportional left ventricular remodeling, and deteriorated cardiac function after MI, indicating that TRPV1 may prevent infarct expansion and cardiac injury by inhibiting inflammation and abnormal tissue remodeling.
Hypertension 2009 Feb
PMID:Transient receptor potential vanilloid gene deletion exacerbates inflammation and atypical cardiac remodeling after myocardial infarction. 1911 47

Combretastatin A-4 phosphate (CA4P) is a novel and promising anti-neoplastic agent. However, it is associated with transient hypertension in both animal and human models. In this study, we examined the potential cardiac toxicity and hypertensive effects of CA4P, and defined the most effective pharmacological inhibition of CA4P-induced hypertension in rats. There was a significant, concentration dependent increase in mean arterial blood pressure with a maximum increase of about 60% of the baseline MAP at 30 mg/kg of CA4P compared to the saline control. However, there was no significant increase in the cardiac troponin I level after CA4P injection. Nitroglycerin and the calcium channel blocker diltiazem effectively blocked the hypertensive effects of CA4P while the beta blocker metoprolol was ineffective. Furthermore, sublingual nitroglycerin administration demonstrated an additional anti-hypertensive effect in a setting of a low dose diltiazem infusion (10 microg/kg/min). We conclude that CA4P treatment resulted in a concentration dependent increase in blood pressure without significant myocardial damage in healthy rats. The hypertensive effect of CA4P was effectively blocked by both nitroglycerin and diltiazem, but not metoprolol.
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PMID:Pharmacological inhibition of the hypertensive response to combretastatin A-4 phosphate in rats. 1973 29

To evaluate whether there is a relationship between admission serum leptin concentrations and peri-operative myocardial injury, 238 consecutive older patients (mean age 81.9+/-7.9 years; 172 women) with low-trauma hip fracture were assessed. Myocardial injury as defined by elevated serum cardiac troponin I was associated with lower leptin levels analyzed as continuous or categorical variables. Patients with serum leptin concentrations <12ng/ml (medium value) had a two-fold greater increased risk for such complications compared with those with higher leptin levels (odd ratio 2.13, 95% confidence interval 1.06-4.28; p=0.033). This association remained significant after adjustments for age, gender, clinical (history of coronary artery disease [CAD], stroke, hypertension, diabetes, dementia), hematological (red, white, and lymphocyte count, hemoglobin, hematocrit), metabolic (parathyroid hormone [PTH], albumin), renal(creatinine, urea, glomerular filtration rate [GFR]), and inflammatory (C-reactive protein [CRP], ferritin) factors. The predictive value of lower leptin levels increased significantly when used in combination with traditional risk factors for myocardial injury.
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PMID:Serum leptin levels in older patients with hip fracture--impact on peri-operative myocardial injury. 1974 42

The present study is the first to utilize bacterial cocaine esterase (CocE) to increase elimination of a lethal dose of cocaine and evaluate its cardioprotective effects. Rats received one of 5 treatments: CocE 1 min after saline; CocE 1 min after a lethal i.p. dose of cocaine; saline 1 min after a lethal i.p. dose of cocaine; CocE immediately after observing a cocaine-induced convulsion; and CocE 1 min after observing a cocaine-induced convulsion. Measures were taken of ECG, blood pressure, and cardiac troponin I (cTnI). The specificity of CocE against cocaine was determined by evaluating its actions against the cocaine analogue, WIN-35,065-2, which lacks an ester attack point for CocE. In addition, CocE's effects were compared with those of midazolam, a benzodiazepine often used to manage cocaine overdose. Whereas CocE alone had negligible cardiovascular effects, it blocked or reversed cocaine-induced QRS complex widening, increased QTc interval, ST elevation, bradycardia, and hypertension. When administered 1 min after cocaine, CocE inhibited myocardial damage; however, administered 1 min after a cocaine-induced convulsion (approximately 40s before cocaine-induced death), CocE did not block cTnI release, but did restore cardiac function. Midazolam blocked convulsions, but exhibited inadequate protection against cocaine-induced cardiotoxicity. The majority of rats given cocaine plus midazolam died. CocE did not prevent the lethal cardiovascular effects of WIN-35,065-2. In all likelihood, CocE rapidly and specifically reduced the body burden of cocaine and inhibited or reversed the cardiovascular consequences of high-dose cocaine. These results support CocE as a potential therapeutic avenue in cocaine overdose.
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PMID:Prevention and reversal by cocaine esterase of cocaine-induced cardiovascular effects in rats. 1980 Jan 83


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