Downstream resistance effects of intracoronary thrombosis in the stenosed canine coronary artery.
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OBJECTIVE: The presence is well established in unstable angina of intracoronary thrombosis in a stenosed epicardial coronary artery. The effects of the thrombus formation on the distal microcirculation are however still unclear. METHODS: We adapted the Folts canine model of left circumflex coronary arterial stenosis and intracoronary thrombosis by the insertion of a pressure catheter distal to the stenosis and by the use of 15 microns radioactive microspheres for measurement of regional myocardial blood flow. This permitted measurement during circumflex artery occlusion of collateral flow, downstream vascular resistance and collateral resistance. RESULTS: Distal circumflex resistance, obtained by dividing the distal circumflex coronary pressure gradient by the collateral flow, significantly increased with thrombosis (94.47 +/- 35.72 to 120.06 +/- 34.47; p = 0.0018) mmHg/ml/min/g. Changes in collateral flow and resistance in the presence of thrombosis, during maximum ischaemic vasodilatation, were inconsistent. CONCLUSION: Thrombosis causes increased vascular resistance in the microcirculation distal to the site of injury. This may be of clinical relevance in unstable angina, characterised by episodes of thrombus growth and embolization, in which ischaemic episodes may be worsened by generalised downstream vascular changes. (+info)
Independent prognostic value of C-reactive protein and troponin I in patients with unstable angina or non-Q-wave myocardial infarction.
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OBJECTIVES: Elevated concentrations of C-reactive protein (CRP), a non-specific acute phase reactant, and troponin I (TnI), a cardiac-specific marker of myocardial damage, have been found to be associated with a higher risk for cardiac events in patients with an acute coronary syndrome. We evaluated CRP alone and in combination with TnI for predicting the incidence of major cardiac complications within 6 months in patients with unstable angina or non-Q-wave infarction (NQMI). METHODS: CRP and TnI was measured on admission in patients with unstable angina or NQMI, but results were kept blinded. Patients were treated according to a conservative management strategy, and the incidence of major cardiac events within 6 months was assessed. RESULTS: An abnormal CRP (> 5 mg/l) and an abnormal TnI (> 0.4 microgram/l) were more frequent in patients that suffered a major cardiac event (CRP: 93 vs. 35%, P < 0.0001; TnI: 73 vs. 26%, P < 0.001). The incidence of major cardiac events was higher in patients with an abnormal CRP than in patients with a normal CRP, both when TnI was abnormal (42 vs. 4.5%, P = 0.003) and when TnI was normal (11 vs. 0%, P = 0.014). Mean event-free survival was excellent in patients with both a normal CRP and TnI, whereas survival was poorest in patients with both an abnormal CRP and TnI (121 +/- 16 vs. 180 days, P < 0.0001). CONCLUSIONS: An abnormal CRP on admission in patients with unstable angina or NQMI is associated with increased incidence of major cardiac events within 6 months, both in patients with normal and abnormal TnI. CRP and TnI have independent and additive prognostic value in this patient group, and the combination may be useful for early risk stratification. (+info)
Prediction of cardiac events after uncomplicated acute myocardial infarction by clinical variables and dobutamine stress test.
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OBJECTIVES: We sought to determine the relative prognostic power of several clinical and dobutamine stress test variables in patients after a first uncomplicated acute myocardial infarction (AMI). BACKGROUND: The value of dobutamine echocardiography (DE) for determining prognosis after AMI is not yet defined. In particular, the influence of dobutamine stress test response on the outcome of these patients is unknown. METHODS: A graded predischarge DE (from 5 to 40 microg/kg/min, plus atropine if needed) was performed in 245 patients (mean age 60 +/- 10 years) with a first uncomplicated AMI. RESULTS: At follow-up (17 +/- 13 months), an adverse outcome occurred in 40 patients: cardiac death in 7, nonfatal myocardial infarction in 9 (hard events = 16) and unstable angina requiring hospital readmission in 24. Significant predictors of adverse outcome by univariate analysis were positive DE, ischemic wall motion score index (WMSI), angina during DE and diabetes for all events, and positive DE, ischemic WMSI and age for hard events. At multivariate analysis, the only independent predictors of adverse outcome were positive DE, diabetes and angina during DE for all events, and positive DE and age for hard events. The presence of both age >60 years and a history of diabetes identified patients at high risk of cardiac events (event rate 37%), compared with patients <60 years and no diabetes (event rate 11%). In patients with intermediate risk (only one clinical risk factor, event rate 18%), DE added prognostic information (event rate 10% in the negatives, 25% in the positives and 35% in the positives with angina). CONCLUSIONS: After uncomplicated AMI, dobutamine stress test variables offer additional prognostic information to clinical data. (+info)
A comparison of troponin T and troponin I as predictors of cardiac events in patients undergoing chronic dialysis at a Veteran's Hospital: a pilot study.
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OBJECTIVE: The purpose of this study was to prospectively evaluate the usefulness of the cardiac troponins as predictors of subsequent cardiac events in patients with chronic renal failure undergoing dialysis. BACKGROUND: Cardiac troponin T (cTnT) and I (cTnI) are cardiac markers that are specific for cardiac muscle. They are also excellent prognostic indicators for patients presenting with chest pain. Although cardiac disease is the leading cause of death in dialysis patients, standard methods to diagnose acute coronary syndromes in patients with renal failure are often misleading. METHODS: A six-month prospective study was done in a university-affiliated Veterans Hospital's dialysis clinic. Forty-nine patients undergoing chronic dialysis with no complaints of chest pain were followed for cardiac events occurring in the six months after cardiac troponin measurements. These included unstable angina, acute myocardial infarction and cardiac death. An additional 83 patients with renal failure but who were not undergoing dialysis were also examined. RESULTS: Within six months all three dialysis patients with elevated cTnI at entry into the study suffered an adverse complication (specificity and positive predictive value = 100%). Twenty-five patients had cTnT elevated at >0.10 ng/ml (53%). Patients with diabetes were more likely to have elevated troponin T levels (64% vs. 25%, p = 0.01). All six patients developing cardiac events within three months had elevations of cTnT >0.1 ng/ml (sensitivity = 100%). Whereas the specificity of cTnT was only 56% for a near-term cardiac event, the negative predictive value of cTnT using a cutoff of < or = 0.1 ng/ml was 100%. On restratifying patients using a cutoff value of cTnT of >0.2 ng/ml, only nine of 49 dialysis patients (18%) had elevated levels. In patients with renal failure not undergoing dialysis, only three of 83 (4%) had elevated troponin I or T. None of these patients suffered a cardiac event in the next six months. CONCLUSIONS: This prospective pilot study clearly delineates the troponins as important prognosticators in asymptomatic otherwise "stable" patients on chronic dialysis, especially those with concomitant diabetes mellitus. It also appears that troponins are more likely to be elevated in dialysis patients than other patients with renal failure not on dialysis. The above suggests that the combination of cTnI and cTnT might be very effective in elucidating cardiac risks of patients with renal failure undergoing chronic dialysis. (+info)
PREDICT: A simple risk score for clinical severity and long-term prognosis after hospitalization for acute myocardial infarction or unstable angina: the Minnesota heart survey.
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BACKGROUND: We evaluated short- and long-term mortality risks in 30- to 74-year-old patients hospitalized for acute myocardial infarction or unstable angina and developed a new score called PREDICT. METHODS AND RESULTS: PREDICT was based on information routinely collected in hospital. Predictors abstracted from hospital record items pertaining to the admission day, including shock, heart failure, ECG findings, cardiovascular disease history, kidney function, and age. Comorbidity was assessed from discharge diagnoses, and mortality was determined from death certificates. For 1985 and 1990 hospitalizations, the 6-year death rate in 6134 patients with 0 to 1 score points was 4%, increasing stepwise to 89% for >/=16 points. Score validity was established by only slightly attenuated mortality prediction in 3570 admissions in 1970 and 1980. When case severity was controlled for, 6-year risk declined 32% between 1970 and 1990. When PREDICT was held constant, 24% of those treated with thrombolysis died in 6 years compared with 31% of those not treated. CONCLUSIONS: The simple PREDICT risk score was a powerful prognosticator of 6-year mortality after hospitalization. (+info)
Enhanced levels of soluble and membrane-bound CD40 ligand in patients with unstable angina. Possible reflection of T lymphocyte and platelet involvement in the pathogenesis of acute coronary syndromes.
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BACKGROUND: The CD40 ligand (CD40L) on activated T cells and platelets may be activating matrix metalloproteinases, inducing procoagulant activity, and be involved in the pathogenesis of acute coronary syndromes by promoting plaque rupture in atheroma. METHODS AND RESULTS: To study the role of CD40L-CD40 interaction in coronary disease, we analyzed levels of soluble (s) and membrane-bound CD40L in the peripheral blood from 29 patients with stable angina, 26 with unstable angina, and 19 controls. Our main findings follow. (1) Patients with unstable angina had significantly raised serum levels of sCD40L when compared with patients with stable angina and controls. (2) Platelets could release large amounts of sCD40L when stimulated ex vivo with the thrombin receptor-agonist peptide SFLLRN in both patients and controls. (3) Platelets in patients with unstable angina were characterized ex vivo by decreased intracellular levels and decreased SFLLRN-stimulated release of sCD40L, which may possibly represent a higher percentage of degranulated platelets in these patients. (4) T cells in patients with unstable angina had enhanced surface expression of CD40L and increased release of sCD40L on anti-CD3/anti-CD28 stimulation in vitro when compared with patients with stable angina and controls. (5) Recombinant CD40L and serum from patients with unstable angina who had high sCD40L levels induced enhanced release of monocyte chemoattractant peptide-1 from mononuclear cells, a CC-chemokine involved in the pathogenesis of atherosclerosis. CONCLUSIONS: This first demonstration of enhanced levels of soluble and membrane-bound forms of CD40L in angina patients, with particularly high levels in patients with unstable angina, suggests that CD40L-CD40 interaction may play a pathogenic role in both the long-term atherosclerotic process and in the triggering and propagation of acute coronary syndromes. (+info)
Prognostic value of maximum ST-vector magnitude during the first 24 h of vectorcardiographic monitoring in patients with unstable angina pectoris.
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AIMS: To assess the prognostic importance of alternate ways of quantifying myocardial ischaemia by continuous ST analysis, the maximum ST vector magnitude and the area under the ST vector magnitude trend curve during the first 24 h of continuous ST monitoring. METHODS AND RESULTS: During a 22-month period from 1991 to 1993, 195 patients admitted to our CCU with suspected unstable angina pectoris, were included in the study. During the first 24 h the patients were monitored for ischaemic episodes with computerized vectorcardiography, using a MIDA 1000 system. Twenty seven (14%) of the 195 patients died or had a non-fatal myocardial infarction within 1 year and the maximum ST vector magnitude among those patients was, on average, 201 microV compared with 118 microV in patients who survived 1 year free of myocardial infarction (P<0.01). The area under the ST vector magnitude trend curve was, on average, 1598 microVmin compared with 164 microVmin (P<0.01). By multivariate analysis, the maximum ST vector magnitude emerged as a superior predictor of death or myocardial infarction, compared with the area under the ST vector magnitude trend curve and the number of ST vector magnitude and ST change vector magnitude episodes. The maximum ST vector magnitude and age were independent predictors of death or non-fatal myocardial infarction within 1 year. CONCLUSION: Maximum ST vector magnitude during the first 24 h of vectorcardiographic monitoring seems to be a strong predictor of subsequent death or non-fatal myocardial infarction. (+info)
Economic assessment of tirofiban in the management of acute coronary syndromes in the hospital setting: an analysis based on the PRISM PLUS trial.
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AIMS: We analysed whether generalized use of tirofiban plus heparin and aspirin might save direct healthcare costs, as compared with heparin and aspirin alone, in patients with acute coronary ischaemic syndromes in Switzerland. METHODS AND RESULTS: We conducted an incremental cost-consequence analysis from the perspective of the admitting hospital for the period of the first 7 days. Costs were analysed for the management of refractory ischaemic conditions and myocardial infarctions, including incremental days on the general ward or intensive care unit, as well as necessary revascularization procedures, and expressed in Swiss francs (CHF) and European currency units (ECU). Drug costs were based on a loading dose of 0.4 micro x kg(-1) x min(-1)and a maintenance dose of 0.1 micro x kg(-1) x min(-1)for tirofiban at a cost of CHF 273.55 (ECU 166.50) per vial. Heparin was administered at a loading dose of 5000 U and a maintenance dose of 1000 U x h(-1). All calculations were standardized to 100 treated patients. The costs of managing ischaemic complications were based on typical practice patterns in Swiss hospitals. The incremental costs per patient of managing unstable angina patients with recurrent ischaemia or myocardial infarction were calculated as CHF 23 325 (ECU 14 198) and CHF 18 599 (ECU 11 321), respectively. The incremental drug costs amounted to CHF 82 065 (ECU 49 954). The additional use of tirofiban resulted in net savings of CHF 54 899 (ECU 33 418) per 100 patients, achieved through a reduction in the cost of treating refractory ischaemic conditions (CHF 79 306, ECU 48 275) and myocardial infarctions (CHF 57 658, ECU 35 097). CONCLUSION: Tirofiban is cost-saving in acute coronary ischaemic syndromes and improves the economics of managing these patients during the initial hospitalization. (+info)