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Biomedical subjects

T M Chou

Publications and source records attributed to T M Chou.

At least 37 records · Page 2Linked to original sources
PubMed1999

Should the electrocardiogram be used to guide therapy for patients with left bundle-branch block and suspected myocardial infarction?

CONTEXT: Recently, an algorithm based on the electrocardiogram (ECG) was reported to predict myocardial infarction (MI) in patients with left bundle-branch block (LBBB), but the clinical impact of this testing strategy is unknown. OBJECTIVE: To determine the diagnostic test characteristics and clinical utility of this ECG algorithm for patients with suspected MI. DESIGN: Retrospective cohort study to which an algorithm was applied, followed by decision analysis regarding thrombolysis made with or without the algorithm. SETTING: University emergency department, 1994 through 1997. PATIENTS: Eighty-three patients with LBBB who presented 103 times with symptoms suggestive of MI. MAIN OUTCOME MEASURES: Myocardial infarction determined by serial cardiac enzyme analyses and stroke-free survival. RESULTS: Of 9 ECG findings assessed, none effectively distinguished the 30% of patients with MI from those with other diagnoses. The ECG algorithm indicated positive findings in only 3% of presentations and had a sensitivity of 10% (95% confidence interval, 2%-26%). The decision analysis showed that among 1000 patients with LBBB and chest pain, 929 would survive without major stroke if all received thrombolysis compared with 918 if the ECG algorithm was used as a screening test. CONCLUSIONS: The ECG is a poor predictor of MI in a community-based cohort of patients with LBBB and acute cardiopulmonary symptoms. Acute thrombolytic therapy should be considered for all patients with LBBB who have symptoms consistent with MI.

Algorithms↗
PubMed1999

Echocardiography in patients with suspected endocarditis: a cost-effectiveness analysis.

PURPOSE: We sought to determine the appropriate use of echocardiography for patients with suspected endocarditis. PATIENTS AND METHODS: We constructed a decision tree and Markov model using published data to simulate the outcomes and costs of care for patients with suspected endocarditis. RESULTS: Transesophageal imaging was optimal for patients who had a prior probability of endocarditis that is observed commonly in clinical practice (4% to 60%). In our base-case analysis (a 45-year-old man with a prior probability of endocarditis of 20%), use of transesophageal imaging improved quality-adjusted life expectancy (QALYs) by 9 days and reduced costs by $18 per person compared with the use of transthoracic echocardiography. Sequential test strategies that reserved the use of transesophageal echocardiography for patients who had an inadequate transthoracic study provided similar QALYs compared with the use of transesophageal echocardiography alone, but cost $230 to $250 more. For patients with prior probabilities of endocarditis greater than 60%, the optimal strategy is to treat for endocarditis without reliance on echocardiography for diagnosis. Patients with a prior probability of less than 2% should receive treatment for bacteremia without imaging. Transthoracic imaging was optimal for only a narrow range of prior probabilities (2% or 3%) of endocarditis. CONCLUSION: The appropriate use of echocardiography depends on the prior probability of endocarditis. For patients whose prior probability of endocarditis is 4% to 60%, initial use of transesophageal echocardiography provides the greatest quality-adjusted survival at a cost that is within the range for commonly accepted health interventions.

Adult↗
PubMed1999

The multicenter study of enhanced external counterpulsation (MUST-EECP): effect of EECP on exercise-induced myocardial ischemia and anginal episodes.

OBJECTIVES: The purpose of this study was to assess safety and efficacy of enhanced external counterpulsation (EECP). BACKGROUND: Case series have shown that EECP can improve exercise tolerance, symptoms and myocardial perfusion in stable angina pectoris. METHODS: A multicenter, prospective, randomized, blinded, controlled trial was conducted in seven university hospitals in 139 outpatients with angina, documented coronary artery disease (CAD) and positive exercise treadmill test. Patients were given 35 h of active counterpulsation (active CP) or inactive counterpulsation (inactive CP) over a four- to seven-week period. Outcome measures were exercise duration and time to > or =1-mm ST-segment depression, average daily anginal attack count and nitroglycerin usage. RESULTS: Exercise duration increased in both groups, but the between-group difference was not significant (p > 0.3). Time to > or =1-mm ST-segment depression increased significantly from baseline in active CP compared with inactive CP (p = 0.01). More active-CP patients saw a decrease and fewer experienced an increase in angina episodes as compared with inactive-CP patients (p < 0.05). Nitroglycerin usage decreased in active CP but did not change in the inactive-CP group. The between-group difference was not significant (p > 0.7). CONCLUSIONS: Enhanced external counterpulsation reduces angina and extends time to exercise-induced ischemia in patients with symptomatic CAD. Treatment was relatively well tolerated and free of limiting side effects in most patients.

Adult↗
PubMed1999

Coronary vasodilator effects of BNP: mechanisms of action in coronary conductance and resistance arteries.

Brain natriuretic peptide (BNP), a hormone secreted predominantly in ventricular myocytes, may influence coronary vascular tone. We studied the coronary vasodilatory response to BNP under physiological conditions and after preconstriction with endothelin-1 (ET-1) in anesthetized pigs. Average peak-flow velocity (APV) was measured using intracoronary Doppler, and cross-sectional area (CSA) was measured using intravascular ultrasound. Coronary blood flow (CBF) was calculated. Intracoronary BNP induced dose-dependent increases in CSA, APV, and CBF similar in magnitude to those induced by nitroglycerin (NTG). The magnitude of BNP-induced vasodilation was accentuated after preconstriction with ET-1. Pretreatment with either the nitric oxide synthase inhibitor Nomega-nitro-L-arginine methyl ester or the cyclooxygenase inhibitor indomethacin attenuated the coronary vasodilator effect of BNP in resistance arteries without influencing epicardial vasodilation. Pretreatment with the ATP-sensitive potassium-channel blocker glibenclamide enhanced epicardial vasodilation in response to BNP. We conclude that BNP exerts coronary vasodilator effects, predominantly in epicardial conductance vessels. An accentuated vasodilatory response to BNP occurs in ET-1-preconstricted arteries. BNP-induced vasodilation in coronary resistance arteries may be partially mediated via nitric oxide and/or prostaglandin release.

Animals↗
PubMed1999

Effects of L-arginine on atherogenesis and endothelial dysfunction due to secondhand smoke.

Secondhand smoke (SHS) and hypercholesterolemia increase cardiovascular risk. We hypothesized that L-arginine, the precursor of nitric oxide (NO), might protect against atherogenesis and endothelial dysfunction caused by SHS. The effects of L-arginine supplementation (2.25% solution ad libitum) and SHS (smoking chambers for 10 weeks) were examined in 32 hypercholesterolemic rabbits. Eight normal rabbits served as controls. Acetylcholine- and nitroglycerin-induced vasorelaxation was assessed in aortic rings precontracted with norepinephrine. Hypercholesterolemia increased intimal lesion area (P=0.012), reduced endothelium-dependent relaxation (P=0.009), and reduced basal (P=0.005) and stimulated (P<0.0005) production of NOs. SHS increased intimal lesion area (P=0. 01) norepinephrine-induced contraction (P=0.001) and reduced endothelium-dependent relaxation (P=0.02). SHS-induced increase in norepinephrine contraction was abolished by the inhibition of NO synthase and removal of endothelium. L-Arginine improved endothelium-dependent relaxation (P=0.001) and attenuated SHS-induced endothelial dysfunction (P=0.007) and atherogenesis (P=0. 001). Basal production of nitrogen oxides correlated inversely with intimal lesion area (r=-0.66; P<0.0005) and stimulated production of NOs correlated with endothelium-dependent relaxation (r=-0.66; P<0. 001). SHS causes endothelial dysfunction and increased adrenergic responsiveness and atherogenesis in hypercholesterolemic rabbits. Chronic dietary supplementation with the NO precursor L-arginine mitigates these effects. The adverse vascular consequences of SHS appear to be mediated via deleterious effects on endothelial function.

Animals↗
PubMed1998

Isolated inferior rectus palsy caused by a metastasis to the oculomotor nucleus.

PURPOSE: To report a case of isolated inferior rectus palsy secondary to a metastasis to the oculomotor nucleus. METHODS: Case report. A 41-year-old woman with a history of breast cancer presented with acute onset of left hypotropia and exotropia. RESULTS: Forced generation testing confirmed weakness of the right inferior rectus muscle that was not reversed by intravenous edrophonium infusion. Magnetic resonance imaging disclosed numerous metastatic lesions to the cerebral hemispheres and brainstem. One lesion in the right midbrain was adjacent to the cerebral aqueduct in the right oculomotor nucleus. CONCLUSION: Metastasis to the oculomotor nucleus is a rare cause of isolated inferior rectus palsy; however, this entity should be considered in the differential diagnosis of an isolated inferior rectus palsy because of the life-threatening consequences of a brainstem lesion.

Adult↗
PubMed1998

In-utero and neonatal exposure to secondhand smoke causes vascular dysfunction in newborn rats.

OBJECTIVES: We sought to determine the effects of secondhand smoke (SHS) exposure on vascular reactivity in newborn and infant rats. BACKGROUND: Secondhand smoke exposure increases cardiovascular risk. Secondhand smoke-induced endothelial dysfunction has been demonstrated in older teenagers and young adults. We have previously shown in adult rabbits that SHS induces atherogenesis and endothelial dysfunction. The effects of SHS on vascular function in the offspring of SHS-exposed mothers and in infants are unknown. METHODS: In this study the effects of in-utero (21 days) and neonatal (28 days) exposure to SHS were examined in 80 rats, 4 weeks of age, in a 2-by-2 design study. Rats were exposed to sidestream smoke in smoking chambers. Aortic rings were excised and isometric force responses to phenylephrine, acetylcholine, A23187 and nitroglycerin were studied in organ baths. RESULTS: Neonatal SHS exposure reduced animal weight (p=0.009). In-utero exposure increased the sensitivity (decreased the EC50) of aortic rings to phenylephrine (p < 0.0005), as did neonatal exposure (p=0.01). Maximal contraction to phenylephrine was reduced by in-utero exposure (p=0.04). In-utero SHS exposure reduced maximal endothelium-dependent relaxation to acetylcholine (p=0.04) and increased the EC50 (p=0.05), suggesting impaired sensitivity to acetylcholine. In-utero exposure decreased the sensitivity (increased the EC50) to the endothelium-independent vasodilator nitroglycerin (p=0.003). CONCLUSIONS: Secondhand smoke has detrimental effects on vascular smooth muscle function in the newborn.

Acetylcholine↗
PubMed1998

Antioxidant diet preserves endothelium-dependent vasodilatation in resistance arteries of hypercholesterolemic rabbits exposed to environmental tobacco smoke.

Environmental tobacco smoke (ETS) has been shown to impair endothelium-dependent vasodilation in vitro. This study was performed to investigate the effect of ETS on acetylcholine (ACh)-mediated blood pressure changes in vivo. Seventeen New Zealand White rabbits were fed a cholesterol diet (0.3%) for 13 weeks. Ten animals were exposed to ETS for 6 h/day, and seven animals were not exposed to ETS (non-ETS). Four of the ETS and three of the non-ETS-exposed rabbits received an antioxidant vitamin diet before and during their cholesterol diet for 21 weeks. Six rabbits served as healthy controls. To determine endothelium-dependent and independent blood pressure (BP) responses, BP was measured through a Tygon catheter, inserted into the right carotid artery at baseline and after each of three incremental intravenous doses of norepinephrine (NE; 1, 4, and 20 microg/kg), ACh (3.3, 10, and 30 microg/kg), and nitroglycerin (NTG; 1, 10, and 40 microg/kg). After NE, BP increases were significantly attenuated in the ETS group (p = 0.001) but not in animals receiving the antioxidant supplement. At both the middle and high ACh concentrations, ETS (p = 0.03 and p = 0.01, respectively) and hypercholesterolemia (p = 0.03 and p = 0.06, respectively) attenuated ACh-induced reductions in BP. At the highest ACh concentration, vitamins enhanced the reduction in BP (p = 0.002) and blocked the effect of ETS (p = 0.04). Neither ETS nor vitamins influenced NTG-induced decreases in BP. A combined antioxidant-vitamin diet can preserve endothelium-dependent vasodilatation in the hypercholesterolemic rabbit exposed to ETS.

Acetylcholine↗
PubMed1998

Revascularization in coronary artery disease. A review of randomized trial data.

Since the advent of bypass surgery in the late 1960s and catheter-based intervention in the late 1970s, the treatment of coronary artery disease has been revolutionized by the concept of revascularization. Surveys have demonstrated that the practice patterns around the world and within the US are inconsistent for these important treatment options and are often driven by availability and economics rather than evidence-based data. In addition, the studies examining the use of medical therapy, balloon angioplasty, atherectomy, coronary stenting, and bypass surgery are consistently lagging behind the technological advances in this field. This article reviews the data that randomized trials and meta-analyses provide to compare these modalities. We attempt to provide a framework for reasoned clinical decision making to help guide patient care. While the breakpoints between the medicine bottle, cath lab, and operating room will continue to evolve, we offer a revascularization strategy for patient subgroups based on what clinical data supports.

Angioplasty, Balloon, Coronary↗
PubMed1998

12-lead ST-segment monitoring vs single-lead maximum ST-segment monitoring for detecting ongoing ischemia in patients with unstable coronary syndromes.

BACKGROUND: 12-lead ECG monitoring of the ST segment is more sensitive than patients' symptoms for detecting ischemia after thrombolytic therapy or catheter-based interventions, but it is unclear whether monitoring of the single lead showing maximum ST deviation would be as efficacious. OBJECTIVE: To determine whether monitoring all 12 ECG leads for changes in the ST segment is necessary to detect ongoing ischemia in patients with unstable coronary syndromes. METHODS: Continuous 12-lead ST segment monitoring was performed in 422 patients from the onset of myocardial infarction or during balloon inflation in catheter-based interventions until the patient's discharge from the cardiac care unit. Computer-assisted techniques were used to determine (1) which lead showed the maximum ST deviation at the onset of myocardial infarction or during balloon inflation and (2) what proportion of later ischemic events were associated with ST deviation in this lead. RESULTS: The lead with the maximum ST deviation could be determined in 312 patients (74%). The remaining 110 (26%) had non-Q wave infarction without ST deviation or no ST changes during balloon inflation. During 18,394 hours of 12-lead ST monitoring, 118 (28%) of the 312 patients had a total of 463 ischemic events, 80% of which were silent. Of 377 ischemic events in which a maximum ST lead was detected, 159 (42%) did not show ST deviation in this lead (sensitivity, 58%; 95% CI, 53%-63%). Routine monitoring of leads V1 and II showed ST deviation in only 152 of the 463 events (sensitivity, 33%; 95% CI, 29%-37%). CONCLUSIONS: Monitoring of all 12 ECG leads for changes in the ST segment is necessary to detect ongoing ischemia in patients with unstable coronary syndromes.

Aged↗
PubMed1997

Physiological concentrations of estradiol attenuate endothelin 1-induced coronary vasoconstriction in vivo.

BACKGROUND: Estrogens are cardioprotective hormones and are reported to have antianginal properties. We examined the effect of physiological concentrations of 17beta-estradiol on coronary reactivity in anesthetized female farm pigs. METHODS AND RESULTS: Epicardial coronary cross-sectional area (CSA) was assessed by two-dimensional intravascular ultrasound, average coronary peak flow velocity (APV) by intravascular Doppler velocimetry, and coronary blood flow (CBF) was calculated. Dose-response curves to intracoronary endothelin-1 (ET-1, 1 pmol/L to 10 nmol/L), the selective ET(B) receptor agonist sarafotoxin (1 pmol/L to 10 nmol/L), and serotonin (0.1 nmol/L to 1 micromol/L) were assessed before and after a 10-minute infusion of intracoronary estradiol (1 nmol/L). Before estradiol administration, ET-1 induced significant dose-dependent decreases in CSA, APV, and CBF. Estradiol attenuated ET-1-induced epicardial vasoconstriction (P<.001) as well as ET-1-induced decreases in APV (P=.05) and CBF (P=.012). In an additional five pigs, vehicle (DMSO) had no effect on ET-1-induced coronary vasoconstriction. Before estradiol administration, sarafotoxin induced no net change in CSA but induced increases in APV and CBF, the extent of which did not change significantly after estradiol. Serotonin induced small decreases in CSA but increased APV and CBF. Estradiol did not influence serotonin-induced changes in CSA, APV, or CBF. CONCLUSIONS: We conclude that estradiol attenuates ET-1-induced vasoconstriction, possibly through effects on the ET(A) receptor, because selective ET(B) receptor-induced stimulation with sarafotoxin remained unchanged. Such an effect on the ET(A) receptor may relate to the antianginal properties of estrogens.

Animals↗
PubMed1997

Premature coronary artery disease associated with a disruptive mutation in the estrogen receptor gene in a man.

BACKGROUND: While estrogens protect against coronary artery disease in women, it is unclear whether they influence cardiovascular function in men. The present report describes coronary vascular abnormalities and the lipoprotein profile of a male patient with estrogen insensitivity caused by a disruptive mutation in the estrogen-receptor gene. METHODS AND RESULTS: Stress thallium scintigraphy, echocardiography, and electron-beam computed tomography (CT) scanning of the coronary arteries and detailed lipoprotein analysis were performed. Electron-beam CT scanning of the coronary arteries showed calcium in the left anterior descending artery. Lipoprotein analysis showed relatively low levels of total (130 mg/dL), LDL (97 mg/dL), and HDL (34 mg/dL) cholesterol; apolipoprotein A-I (91.7 mg/dL); and lipoprotein(a) (4.1 nmol/L), but normal levels of triglycerides (97 mg/dL) and pre-beta-1-HDL cholesterol (61 microg/mL). CONCLUSIONS: The absence of functional estrogen receptors may be a novel risk factor for coronary artery disease in men.

Adult↗