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Biochemical markers are useful for the prediction of future cardiovascular events in patients with non-ST-segment elevation acute coronary syndrome (ACS). The independent as well as the combined prognostic value of elevated troponin-T, high-sensitivity C-reactive protein (hs-CRP), and N-terminal pro-brain natriuretic peptide (NT-pro-BNP) on the Thrombolysis In Myocardial Infarction (TIMI) risk score and on the short-term prognosis were evaluated in a cohort of ACS patients.In an unselected, heterogeneous group of 80 patients with ACS (i.e., unstable angina [USA] or non-ST-elevation myocardial infarction [NSTEMI]), the levels of troponin-T, hs-CRP, and NT-pro-BNP were analyzed. The correlation between elevation of different biomarkers with TIMI risk score and their impact on 30-day major adverse cardiac events was sought. The levels of hs-CRP were significantly higher in patients who had angina as their predominant complaint (3.67 mg/dl vs. 1.67 mg/dl: p0.01), while levels of NT-pro-BNP was higher in those patients who had any element of heart failure at presentation (2616.39 pg/ml vs. 1068.3 pg/ml; p0.01). Troponin-T was highest in patients who had an element of both heart failure and angina at presentation (p0.01). The TIMI risk score expectedly had a positive and strong correlation with elevated troponin-T, but had no correlation with elevation of hs-CRP and NT-pro-BNP in isolation. However, when any two biomarkers were elevated, the patients were in the intermediate risk group as per TIMI risk score irrespective of troponin-T-elevation. When all the three biomarkers were elevated, the risk equaled the high-risk category of TIMI risk score. Elevated hs-CRP (3.40 mg/dl vs. 1.38 mg/dl; p0.001) and troponin-T (2.37 ng/ml vs. 1.23 ng/ml; p0.001) at baseline correlated independently with the occurrence of re-ischemia, while elevated NT-pro-BNP alone correlated significantly with the development of heart failure within 30 days of follow-up (4247.76 pg/ml vs. 1210.86 pg/ml; p0.01). The highest risk of death from any cardiovascular cause within 30 days of follow-up was significantly higher when all the three biomarkers were elevated.The use of NT-pro-BNP, hs-CRP, and troponin-T in combination appears to add critical prognostic insight to the assessment of patients with ACS.

Left ventricular pacing is increasingly being used as a part of biventricular pacing in congestive heart failure but data on safety, feasibility, reliability and lead maturation are sparse.Seventeen patients (13 males and 4 females) with persistent symptomatic degenerative complete heart block underwent temporary left ventricular pacing by a left subclavian puncture through the coronary sinus to its tributaries using a unipolar permanent pacing lead connected to an external pulse generator. The left ventricular pacing was done for two weeks. Permanent right ventricular apical pacing was also done at the same time through a right cephalic vein cut-down or subclavian puncture and the pacing rate was kept below that of the initial left ventricular pacing rate. Pacing parameters of the left and right ventricles were assessed at the time of implantation and at two weeks. Out of 17 patients, left ventricular pacing was successful in 11 (67.7%) patients. The time taken for the total procedure was 56+/-18.1 min. Lead displacement was noted in one patient without loss of pacing. At the time of implant and after two weeks, left ventricular pacing threshold, impedance, R wave height and slew rate were not different as compared to right ventricular pacing. Holter recording for 24 hours revealed regular left ventricular pacing at the end of two weeks in all patients.The present study shows that left ventricular pacing through coronary sinus tributaries is feasible and reliable. Acute and subacute maturation of left ventricular pacing are similar to right ventricular apical pacing.

The present study was undertaken to assess the impact of megadose heparin bolus on angiographic patency of infarct-related artery in patients of acute myocardial infarction presenting between 7-12 hours and to compare it with streptokinase. Forty-seven patients (27 males, mean age 58.1 +/- 9.6 years) of acute myocardial infarction between 7-12 hours of onset of chest pain were randomised to receive either megadose heparin bolus (300 IU/kg body weight, group 1, n = 24; or streptokinase 1.5 million units over one hour, group 2, n = 23). Parameters noted were: relief of pain at 90 minutes, 50 percent or more resolution of ST segment at 90 minutes, TIMI grade flow and left ventricular ejection fraction at discharge. Mean age (59.0 +/- 12.9 years in group 1; 57.2 +/- 8.1 years in group 2), mean time to drug (7.5 +/- 1.3 hours in group 1; 7.8 +/- 1.6 hours in group 2), site of anterior wall infarction (12 in group 1, 10 in group 2), relief of pain at 90 minutes (15 in group 1, 14 in group 2) and more than 50 percent resolution of ST segment elevation at 90 minutes (12 patients in each group) were similar. On coronary angiography performed in 42 patients (21 in each group) at a mean interval of 7.2 +/- 1.3 days after acute myocardial infarction, TIMI grade 3 flow was seen in 7 (33.3%) patients in each group and TIMI grade 2/3 flow was also similar in both the groups (p = NS). No major bleed occurred in either group. We conclude that heparin given as a megadose bolus produces similar TIMI 3 flow in infarct-related artery as compared to streptokinase in acute myocardial infarction patients presenting between 7-12 hours.

Bolus followed by rapid infusion of tissue plasminogen activator results in higher grade of TIMI flow in infarct-related artery as compared to slow infusion. In the present study, an accelerated regimen of streptokinase given over 15 minutes was compared with conventional infusion over one hour in 47 patients presenting within 12 hours of acute myocardial infarction. Forty-seven patients (44 males, 3 females; mean age 54.0 +/- 1.1 years) were randomly allocated to receive 1.5 million units of streptokinase either over 15 minutes (group 1, n = 24) or over one hour (group 2, n = 23) at a mean interval of 5.4 +/- 3.6 hours after onset of symptoms. All the patients received aspirin and intravenous heparin (1000 U/hr) for 96 hours after thrombolysis. Coronary angiography was performed in 43 patients (22 in group 1, 21 in group 2) prior to discharge from the hospital (mean 7 +/- 2.1 days after acute myocardial infarction) and patency of the infarct-related artery and grade of TIMI flow were determined. Infarct-related artery was patent (TIMI 2/3 flow) in 19 (86.4%) patients in group 1 as compared to 12 (57.1%) in group 2 (p0.05). TIMI grade 3 flow in the infarct-related artery was present in 13 (59.1%) in group 1 as compared to 7 (33.3%) in group 2 (p = 0.1). There was no significant difference between group 1 and 2 in time of presentation (mean 5.3 +/- 3.9 hrs vs 5.5 +/- 3.2 hrs), time to needle in hospital (25.6 +/- 11.2 min vs 26.3 +/- 6.2 min), site of infarct (anterior myocardial infarction 12 in group 1 vs 11 in group 2), relief of pain at 90 min (13 vs 12), more than 50 percent reduction of ST elevation at 90 minutes (17 vs 12) and left ventricular ejection fraction (48.8 +/- 9.1% vs 49.8 +/- 16.0%), respectively. Streptokinase was well tolerated in both the groups, although hypotension was more common with the accelerated regimen (5 in group 1 vs 3 in group 2; p = NS). Thus, 'accelerated' streptokinase given over 15 minutes in patients presenting within 12 hours of acute myocardial infarction is well tolerated and results in higher grades of TIMI flow in the infarct-related artery as compared to the "conventional" one-hour infusion regimen.

Eighteen patients of 'Q' wave acute myocardial infarction (AMI) (age 50 +/- 6.2 years), underwent dobutamine stress echocardiography (DSE) before hospital discharge (7.2 +/- 1.3 days after AMI) to find out the correlation between response of infarct zone to dobutamine infusion and TIMI grade flow in infarct related artery (IRA). The aim of study was to test the hypothesis that infarct zone which shows improvement in contractility after dobutamine infusion has viable myocardial tissue and would have good flow (TIMI II or III) in IRA. Echocardiographically, improvement in contractility in the centre of infarct zone by at least 1 grade (on a scale of 4) was termed as positive response on DSE. The mean dose of dobutamine was 19.4 micrograms/kg/min. Ten patients had positive response on DSE; 8 of them had good antegrade flow in IRA. Eight patients had no improvement in contractility of infarct zone on DSE; 6 of them had poor flow in IRA. Clinical markers of reperfusion (relief of chest pain, early ST settlement, peak CPK-MB levels), age of patient, site of AMI, time to thrombolysis, resting left ventricular ejection fraction, wall motion score of the infarct zone and presence of collaterals were not significantly different in patients with good or poor flow in IRA. Thus, improvement in contractility of infarct zone after dobutamine infusion can predict good flow (TIMI II or III) in IRA with 80 percent sensitivity, 75 percent specificity, 80 percent diagnostic accuracy, 80 percent positive predictive value and 75 percent negative predictive value.

In this double blind randomised placebo controlled study, we investigated the antianginal efficacy of oral captopril in 33 patients of angiographically documented coronary artery disease (chronic stable angina). Apart from sublingual nitrates, all other antianginal drugs were withdrawn. Patients were then evaluated both subjectively by questionnaire and objectively by treadmill stress test. No patient had more than mild hypertension and all patients had good left ventricular function. One group of patients received oral captopril while the other group was given placebo. A repeat assessment was done after six weeks and the results compared with baseline. Anginal attacks decreased from 20.11 +/- 1.86 per week on placebo to 9.92 +/- 1.38 (p0.01) on captopril as also the number of sublingual nitrates (18.84 +/- 3.01 to 11.14 +/- 2.94, p0.01). Assessment by the treadmill stress test showed that in comparison to the pretreatment test, captopril therapy resulted in a significantly increased exercise duration (6.26 +/- 0.21 to 6.98 +/- 0.31 minutes, p0.05), total work done (6.76 +/- 0.26 METS to 7.48 +/- 0.29 METS, p0.05). In addition there was a significant increase in time to angina (6.16 +/- 0.18 to 6.85 +/- 0.24 min, p0.05) and time to 1mm ST depression (5.18 +/- 0.26 to 6.46 +/- 0.30 min, p0.01). We conclude that captopril is an effective monotherapy for patients with chronic stable angina and has both antianginal as well as anti-ischemic effects, possibly secondary to direct coronary vasodilation.

Acute respiratory failure evolved in five patients following hypovolemic shock related to trauma or surgical operation, or both. A reduction in colloid osmotic pressure, increases in pulmonary artery wedge pressure and reductions in colloid osmotic pressure-pulmonary artery wedge pressure gradient to levels which are likely to account for pulmonary edema were observed. Accordingly, reduction in the colloid hydrostatic pressure gradient may, in part, explain the development of acute respiratory failure after acute blood loss. In one instance, however, the absence of such reduction in the colloid osmotic pressure-pulmonary artery wedge pressure gradient together with increases in pulmonary vascular resistance showed that colloid osmotic pressure and pulmonary artery wedge pressure are not exclusively operative in the pathogenesis of the clinical syndrome of acute respiratory failure.

The in vitro effect of prostaglandin E1 on the fibrinolytic process was assessed in 30 patients with acute myocardial infarction (MI) using Thrombin Time (TT) and Euglobulin Clot Lysis time (ECLT) as parameters. Thrombin time was shortened and ECLT was prolonged (p less than 0.001) in acute MI as compared to thirty age and sex matched controls. In both groups, preincubation of sera with PGE1 (3.3 micrograms/ml) produced prolongation of TT and shortening of ECLT (p less than 0.001). Thus PGE1, which is a naturally occurring vasodilator and antiplatelet agent, also appears to have fibrinolytic activity.

A patient is presented in whom pulmonary artery catheter insertion fortutiously demonstrated persistent left superior vena cava on two separate occasions. Further studies with venogram and a first pass nuclear scan demonstrated total absence of the right superior vena cava. Although this anomaly is commonly associated with intracardiac defects and rhythm disturbances only the latter was seen in our patient. Invasive hemodynamic monitoring is frequently performed in the majority of modern intensive care units. The bedside technique used for insertion of a Swan-Ganz catheter using only pressure monitoring for advancing the catheter has relatively few complications. One such complication is misplacement along an anomalous route where the catheter may take to the heart. We have recently treated a patient on two separate occasions who had a persistent left superior vena cava with absent right superior vena cava.