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BackgroundThere is no method of quantifying the severity of mitral regurgitation (MR) from injection of tracer directly into the left ventricular (LV) cavity, a method commonly used in the cardiac catheterization laboratory. Methods and ResultsWe used a previously validated mathematical model that derives regurgitant fraction (RF) from the relative tracer washout from the left atrial (LA) and LV cavities. Thirty-nine patients referred for diagnostic cardiac catheterization with clinical evidence of possible MR were included in the study. Five milliliters of a microbubble mixture was power-injected into the LV during simultaneously performed contrast echocardiography. Relative changes in background-subtracted video intensity were measured from the LV and LA, and the resultant model-derived RF was correlated with the severity of MR on cineangiography. The severity of MR ranged from 0 to 4+ on cineangiography with corresponding model-derived RF of 0 to 0.69 on contrast echocardiography. A close linear relation was noted between angiographic severity of MR and model-derived RF on contrast echocardiography (y= 0.1x+ 0.03, r= 0.89, P<.001). Contrast echocardiography was more sensitive than cineangiography for detecting mild MR. ConclusionsWe describe a new method of measuring the severity of MR in the cardiac catheterization laboratory. Apart from being quantitative, this method can be safely used during cardiac catheterization in patients in whom iodinated contrast agents may be potentially harmful. (Am Heart J 2000;139:1109-13.)

BackgroundThrombus is important in the pathophysiology of several complications of angioplasty, including abrupt closure and restenosis. Levels of prothrombin fragment F1.2 and fibrinopeptide A reflect thrombin generation and activity. The effect of angioplasty on levels of these markers is unclear. MethodsPatients undergoing either balloon angioplasty (n = 30) or directional atherectomy (n = 9) were treated with heparin to maintain an activated clotting time of >300 seconds. Levels of F1.2, fibrinopeptide A, and thrombin-antithrombin complex were measured in the coronary sinus and coronary artery before and after intervention. Angiograms were reviewed for lesion morphologic characteristics and dissection. ResultsThere was no evidence for thrombin generation or increased thrombin activity after angioplasty regardless of lesion morphologic characteristics, dissection, type of intervention, or blood sampling site. In fact, coronary sinus concentrations of F1.2 decreased after intervention (median 0.31 nmol/L; 25th percentile 0.26 nmol/L, 75th percentile 0.37 nmol/L) before intervention to 0.23 nmol/L (25th percentile 0.19 nmol/L, 75th percentile 0.34 nmol/L) after intervention (P=.002). ConclusionsAngioplasty performed in the presence of adequate heparin inhibited thrombin even when there was complex lesion morphology or dissection. These data suggest that heparin provides satisfactory thrombin inhibition during routine angioplasty. (Am Heart J 1999;137:250-7.)

To assess the efficacy of intravenous streptokinase in patients with acute myocardial infarction, 40 patients (30 men and 10 women, mean age 54 years) with acute myocardial infarction were given 1.5 million U of streptokinase intravenously in 1 hour, and coronary arteriography was performed repeatedly to assess reperfusion. Streptokinase treatment was begun 270 ± 86 (mean ± SD) minutes after the onset of chest pain. Of the 40 patients, 34 had total or near total coronary occlusion before streptokinase administration. In 14 (41%) of these 34 patients, some reperfusion occurred during the 90 minutes after the administration of streptokinase, but in only 11 of the 14 was reperfusion present at 90 minutes. After streptokinase administration, all patients received heparin for 8 to 10 days; they were subsequently administered aspirin and dipyridamole. Clinical evidence of reocclusion during the first 24 hours of heparin therapy occurred in one patient. Thus, when given to patients with acute myocardial infarction and total coronary occlusion an average of 4½ hours after the onset of chest pain, high dose intravenous streptokinase achieves reperfusion in only about 40% and results in sustained reperfusion in only about 30%.

A randomized, parallel, double-blind study was performed with lisinopril, a long-acting angiotensin-converting enzyme inhibitor, versus captopril, a shorter-acting angiotensin-converting enzyme inhibitor, in the treatment of congestive heart failure. All patients were in New York Heart Association class II, III or IV and had remained symptomatic despite therapy with digoxin and diuretics. After a 4 to 14 day placebo baseline period, patients were randomized to receive either lisinopril, 5 mg orally once per day (n = 94), or captopril, 12.5 mg orally three times per day (n = 95), in addition to continuation of digoxin and diuretics. The dose of study drug could be doubled at 4 week intervals for a total of 12 weeks of double-blind therapy. The maximal dose was 20 mg once per day of lisinopril or 50 mg three times per day of captopril.

The effect of balloon size on the success of coronary angioplasty was studied to develop quantitative criteria for optimal selection of balloon size. Coronary dimensions of 165 stenotic lesions were measured by computer-assisted cinevideodensitometry in 120 patients who had undergone angioplasty with a balloon selected by visual estimates. Cross-sectional areas and diameters of normal and stenotic arterial segments were measured before and after angioplasty by a previously validated cinevideodensitometric technique. The diameter of the inflated balloon compared with that of the normal arterial segment was expressed as a ratio for sizing balloons.

This study was conducted in human subjects and in baboons to assess elements of the β-adrenergic receptor complex in vivo and in vitro following cardiac transplantation. In human subjects, the concentration at which administered isoproterenol increased heart rate by 25 beats per min was within the normal range (mean, 3.2±0.4 μg). Myocardial biopsies and lymphocytes were obtained from 14 transplant recipients undergoing routine right heart catheterization. The stimulatory guanine nucleotide regulatory protein, Gs, was significantly greater in the lymphocyte than in right ventricular myocardium (5.8±1.7 vs. 2.0±0.5 relative to standard rat heart membrane preparation, P<0.05). In contrast, Gi was significantly greater in the myocardium than in the lymphocyte (4.2±1.3 vs. l.l±0.3, P<0.025). There was no correlation between lymphocyte and cardiac G protein determinations.

This study was designed to examine the effect of increases in the partial pressure of carbon dioxide (Pco2) in coronary artery blood on coronary blood flow, coronary reactive hyperemia and the coronary response to intra-coronary adenosine administration. The left anterior descending coronary artery was cannulated and perfused over a wide range of perfusion pressure (P) and flow (F) with blood equilibrated with 0 to 40% carbon dioxide in 16 open chest dogs. Increases in coronary artery Pco2from 20 ± 2 to 93 ± 8 to 211 ± 22 mm Hg (mean ± SEM) increased the coronary flow from 28 ± 3 to 68 ± 16 to 87 ± 22 ml/min, respectively, at a perfusion pressure of 60 mm Hg and from 49 ± 6 to 139 ± 30 to 206 ± 48 ml/min, respectively, at a perfusion pressure of 100 mm Hg.

We have determined the plasma level of fibrinopeptide A as a specific index of thrombin activity during the infusion of a thrombolytic agent in patients with acute myocardial infarction. Peripheral venous plasma levels of fibrinopeptide A increased following the initiation of thrombolytic therapy from 2.7 nmol/L to a peak of 13.0 nmol/L at 30 minutes with streptokinase and from 1.1 nmol/L to a peak of 10.7 nmol/L at 90 minutes with tissue plasminogen activator. The amount of fibrinogen converted to fibrin I was determined by integration of the plasma level of fibrinopeptide A over time. The amount of fibrin I formed over the five-hour period from the start of drug infusion was approximately 10 mg/dL in response to either streptokinase or recombinant tissue plasminogen activator. We conclude that activation of coagulation occurs in response to thrombolytic therapy despite heparin administration. This thrombin action, though transient, would be sufficient to cause rethrombosis if localized and incompletely opposed by fibrinolytic activity. © 1988 by Grune & Stratton, Inc.

The article presents information on the 2015 Go Red For Women cardiovascular health awareness campaign of the American Heart Association Lowcountry sponsored by the Medical University of South Carolina.

Thrombin may play a central role in restenosis after balloon angioplasty (BA), and angiographic and pathologic restenosis have been shown to be reduced in the rabbit model using recombinant desulfatohirudin, a selective thrombin inhibitor. We hypothesized that an intravenous infusion of hirulog, a 20 amino acid potent and selective thrombin inhibitor, given at the time of angioplasty would reduce restenosis in the atherosclerotic rabbit model. Focal femoral atherosclerosis was induced in 27 rabbits by air desiccation endothelial injury followed by a 2% cholesterol diet for 1 month. At BA (2.5mm balloon with three 60-second, 10 atm inflations 60 seconds apart), rabbits received either heparin (150 units/kg bolus, n=14) or hirulog (5mg/kg bolus followed by 5mg/kg/hr × 2 hours, n=13). Angiograms performed before and after BA and at 28 days were analyzed quantitatively by two blinded observers. Rabbits were sacrificed 28 days after BA, and quantitative histomorphometric analysis was performed on all vessels. The angiographic mean luminal diameters (LD) in mm were:Pre-BAPost-BA28 DaysHeparin1.1±0.21.5±0.2*1.0±0.4*†Hirulog1.2±0.11.6±0.1*1.5±0.2†*p=&lt;0.05 pre vs post, post vs 28 days†p=0.0001 heparin vs hirulog at 28 days

The article presents an open letter from Eric R. Powers, cardiologist and Co-Medical Director at Hearts Vascular Center at the Medical University of South Carolina about the women's heart care program at the center.

The author discusses the Medical University of South Carolina's (MUSC) sponsorship of the American Heart Association Lowcountry Go Red For Women campaign for 2013. The campaign makes use of the energy, passion and power of women to band together and collectively work to eliminate heart disease. An overview of the women's heart care program at the MUSC Heart & Vascular Center is provided.