Association between diarrhoea and shedding of group A and atypical groups B to E rotaviruses in suckling pigs.

The frequency of shedding of rotavirus in faeces of diarrhoeic piglets was studied in 2 farms. In farm I, where 82% of the litters had diarrhoea, group A rotavirus was detected in 52/117 (44%) faeces of pigs with diarrhoea while atypical groups B to E rotaviruses were detected in 2/117 (2%) faeces of diarrhoeic piglets that came from litters where group A rotavirus had also been found. In farm II where the morbidity due to diarrhoeas was lower (57% of the litters had diarrhoea), 8/141 (6%) faeces of piglets with diarrhoea had group A rotavirus and 4/141 (3%) had groups B to E atypical rotaviruses. It was concluded that group A and groups B to E rotaviruses can coexist in the same farm but group A rotavirus seems to induce more diarrhoeas in piglets.

Effect of cocaine on coronary artery dimensions in atherosclerotic coronary artery disease: enhanced vasoconstriction at sites of significant stenoses.

Cocaine increases myocardial oxygen demand and paradoxically decreases oxygen supply by reducing coronary blood flow. Such "inappropriate" vasoconstriction also occurs with exercise, which causes intense vasoconstriction of coronary artery segments narrowed by atherosclerosis. This study was done to assess the cocaine-induced change in vasomotor tone of diseased and nondiseased coronary artery segments. In 18 patients (15 men, 3 women, aged 35 to 67 years), coronary artery areas in diseased and nondiseased segments were quantitated before and 15 min after administration of intranasal saline solution (6 patients) or cocaine (2 mg/kg body weight) (12 patients). No variables changed after intake of the saline solution. In response to cocaine, the luminal areas of diseased and nondiseased segments decreased, but the magnitude of vasoconstriction was greater in the diseased segments (mean +/- SD 29 +/- 23% versus 13 +/- 8%, p less than 0.05). Thus, cocaine causes vasoconstriction of diseased and nondiseased coronary artery segments, but its effect is particularly marked in the former.

Potentiation of cocaine-induced coronary vasoconstriction by beta-adrenergic blockade.

STUDY OBJECTIVE: To determine whether beta-adrenergic blockade augments cocaine-induced coronary artery vasoconstriction. DESIGN: Randomized, double-blind, placebo-controlled trial. SETTING: A cardiac catheterization laboratory in an urban teaching hospital. PATIENTS: Thirty clinically stable patient volunteers referred for catheterization for evaluation of chest pain. INTERVENTIONS: Heart rate, arterial pressure, coronary sinus blood flow (by thermodilution), and epicardial left coronary arterial dimensions were measured before and 15 minutes after intranasal saline or cocaine administration (2 mg/kg body weight) and again after intracoronary propranolol administration (2 mg in 5 minutes). MEASUREMENTS AND MAIN RESULTS: No variables changed after saline administration. After cocaine administration, arterial pressure and rate-pressure product increased; coronary sinus blood flow fell (139 +/- 28 [mean +/- SE] to 120 +/- 20 mL/min); coronary vascular resistance (mean arterial pressure divided by coronary sinus blood flow) rose (0.87 +/- 0.10 to 1.05 +/- 0.10 mm Hg/mL.min); and coronary arterial diameters decreased by between 6% and 9% (P less than 0.05 for all variables). Subsequently, intracoronary propranolol administration caused no change in arterial pressure or rate-pressure product but further decreased coronary sinus blood flow (to 100 +/- 14 mL/min) and increased coronary vascular resistance (to 1.20 +/- 0.12 mm Hg/mL.min) (P less than 0.05 for both). CONCLUSIONS: Cocaine-induced coronary vasoconstriction is potentiated by beta-adrenergic blockade. Beta-adrenergic blocking agents probably should be avoided in patients with cocaine-associated myocardial ischemia or infarction.

Influence of anterograde flow in the infarct artery on the incidence of late potentials after acute myocardial infarction.

In patients after myocardial infarction, survival is influenced by the presence or absence of anterograde flow in the infarct artery, and late potentials on signal-averaged electrocardiography identify those at risk for tachyarrhythmias and sudden death. To assess the frequency of late potentials in survivors of first infarction, coronary arteriography and signal-averaged electrocardiography were performed in 109 subjects (64 men, 45 women, aged 30 to 77 years), 49 with (group I) and 60 without (group II) anterograde flow in the infarct artery. The groups were similar in age, sex, infarct artery, severity of coronary artery disease and left ventricular function. However, only 4 (8%) of group I had late potentials, whereas 24 (40%) of group II had late potentials (p less than 0.001). Thus, anterograde flow in the infarct artery after myocardial infarction is associated with a low incidence of late potentials on signal-averaged electrocardiography, whereas the absence of anterograde flow is more often associated with late potentials.

Ethanol-induced coronary vasodilation in patients with and without coronary artery disease.

To assess the influence of ethanol on coronary arterial blood flow and dimensions, we measured coronary sinus blood flow in 35 subjects (23 men and 12 women, aged 38 to 69 years; (29 with and 6 without coronary artery disease) before and during a 15- to 30-minute intracoronary infusion of (1) 5% dextrose in water (n = 15, controls) or (2) 5% dextrose in water (n = 20). In the controls heart rate, arterial pressure, and coronary sinus blood flow were unchanged. In those receiving ethanol at a rate that produced a concentration in coronary sinus blood of 285 +/- 102 (mean +/- SD) mg/dl, heart rate-systolic arterial pressure product was unchanged; coronary sinus blood flow rose 27 +/- 36%, and coronary vascular resistance fell 17 +/- 22% (p less than 0.05 in comparison to baseline); arterial-coronary sinus oxygen content difference fell (p less than 0.05), and epicardial coronary arterial dimensions were unchanged. Thus intracoronary ethanol increases coronary blood flow and decreases resistance without inducing a change in epicardial coronary dimensions, suggesting that its effect results from dilatation of the intramyocardial resistance vessels.

Cocaine-induced coronary-artery vasoconstriction.

Intranasal cocaine is used frequently as a local anesthetic during many rhinolaryngologic procedures. Although its "recreational" use in high doses has been associated with chest pain and myocardial infarction, this association has not been established when cocaine is used in low doses as a topical anesthetic, and its effect on the coronary vasculature of humans is unknown. We studied the effects of intranasal cocaine (10 percent cocaine hydrochloride; 2 mg per kilogram of body weight) on the blood flow in and dimensions of the coronary arteries and on myocardial oxygen demand in 45 patients (34 men and 11 women, 36 to 67 years of age) who were undergoing cardiac catheterization for the evaluation of chest pain. Heart rate, arterial pressure, blood flow in the coronary sinus (measured by thermodilution), and the dimensions of the epicardial left coronary artery (measured by quantitative arteriography) were measured before and 15 minutes after the intranasal administration of saline (in 16 patients) or cocaine (in 29). No variables changed after the administration of saline. After cocaine was administered, the heart rate and arterial pressure rose, the coronary-sinus blood flow fell (from a mean [+/- SD] of 149 +/- 59 ml per minute to 124 +/- 53 ml per minute), and the diameter of the left coronary artery decreased by 8 to 12 percent (P less than 0.01 for all comparisons). No patient had chest pain or electrocardiographic evidence of myocardial ischemia after the administration of cocaine. Subsequently, the administration of the alpha-adrenergic blocking agent phentolamine caused all these values to return to base-line levels. There was no difference in response between the patients found to have disease of the left coronary artery (n = 28) and those without such disease (n = 17). We conclude that the intranasal administration of cocaine near the dose used for topical anesthesia causes vasoconstriction of the coronary arteries, with a decrease in the coronary blood flow, despite an increase in myocardial oxygen demand, and that these effects are mediated by alpha-adrenergic stimulation. It is reasonable to assume that these effects would be more pronounced at the much higher doses associated with the recreational use of cocaine.

Quantitative assessment of coronary arterial diameter before and after coronary artery bypass grafting.

Because coronary artery bypass graft patency is related to the size of the artery, a preoperative assessment of arterial diameter is important. However, the relation between coronary arterial diameter (assessed by angiography) and true luminal size of arteries that are occluded and filled by collaterals has not been completely characterized. This study was done to measure the luminal diameter of coronary arteries before and after bypass grafting. Twenty-six patients (20 men and 6 women, aged 34 to 72 years) had coronary angiography before and from 1 to 35 months after bypass surgery. Coronary arterial luminal diameter was similar before and after operation for the 18 insignificantly narrowed arteries and the 24 arteries with narrowings that filled by anterograde flow before operation and were bypassed. In contrast, in the 21 arteries that were occluded and filled by collateral flow, coronary arterial diameter was significantly larger (p less than 0.001) after operation. Thus, when a coronary artery is occluded and filled by collaterals, its true luminal size is consistently underestimated by the angiogram.

Angiographic characteristics of the infarct-related coronary artery in patients with angina pectoris after myocardial infarction.

To elucidate the pathophysiology of angina pectoris after myocardial infarction, we analyzed the coronary stenoses in 45 subjects (28 men, 17 women, aged 33 to 67 years) with recent (less than or equal to 60 days) infarction, significant narrowing of only the infarct-related artery, and residual anterograde flow in this artery. Postinfarction angina was absent in 19 (group I) and present in 26 (group II). The groups were similar in age, left ventricular function, incidence with which each coronary artery was involved, as well as stenosis diameter (1.0 +/- 0.3 vs 0.9 +/- 0.4 mm [mean +/- standard deviation], respectively, difference not significant), stenosis area (0.9 +/- 0.4 vs 0.8 +/- 0.8 mm2, respectively, difference not significant), percent diameter narrowing (65 +/- 5 vs 66 +/- 9, respectively, difference not significant), and stenosis eccentricity. However, those with postinfarction angina had longer stenoses (group I, 4.3 +/- 1.4 mm; group II, 10.3 +/- 4.0 mm; p less than 0.001). Thus, patients with postinfarction angina and residual anterograde flow in the infarct artery may have angina due to a marked reduction in anterograde flow, caused by a long stenosis. There is no apparent relation between stenosis eccentricity and postinfarction angina.

Prognosis after acute myocardial infarction in patients with and without residual anterograde coronary blood flow.

The restoration of anterograde coronary flow during the hours to days after acute myocardial infarction (AMI) may be beneficial independent of an effect on left ventricular function. This study was done to assess the influence of residual anterograde coronary perfusion on long-term morbidity and mortality in patients after AMI. Over a 10-year period, 179 subjects (132 men, 47 women, aged 25 to 66 years) with infarction and angiographic evidence of disease of only 1 coronary artery were followed for 47 +/- 29 (mean +/- standard deviation) months. All were receiving medical therapy. Sixty-four patients had partial or complete anterograde perfusion of the infarct artery (group I), whereas the other 115 had no or minimal anterograde perfusion (group II). The 2 groups were similar in age, sex, risk factors for atherosclerotic cardiovascular disease, duration of follow-up, maintenance medications and left ventricular function. In group I, unstable angina and congestive heart failure each occurred in less than or equal to 10%, and none died. In marked contrast, the 115 patients in group II frequently had unstable angina (25%) and congestive heart failure (17%) (p less than or equal to 0.05 for both vs group I), and 21 (18%) died suddenly (p less than 0.001 vs group I). Thus, the incidence of long-term morbidity and mortality is greatly increased after AMI in patients without residual anterograde perfusion of the infarct-related coronary artery. In these patients, the restoration of partial or complete anterograde flow--pharmacologically or mechanically--may be beneficial even if it is accomplished hours to days after the acute event.

Dosing of contrast material to prevent contrast nephropathy in patients with renal disease.

PURPOSE: Contrast-induced renal dysfunction has been reported to occur in 15% to 42% of patients with underlying azotemia, but there is disagreement as to whether its incidence is reduced by limiting the amount of contrast material. To adjust the amount of contrast material to the severity of azotemia, we have utilized the following formula to calculate a contrast material "limit" in patients with renal disease: Contrast material limit = (formula; see text) PATIENTS AND METHODS: Over a 10-year period, 115 patients (53 men, 62 women, aged 61 +/- 11 [mean +/- SD] years) with renal dysfunction (baseline serum creatinine level greater than or equal to 1.8 mg/dL) underwent cardiac catheterization and angiography, after which the level of serum creatinine was measured daily for five days. The amount of contrast material that was given adhered to the limit in 86 patients (Group I) and exceeded it in 29 (Group II). RESULTS: Contrast-induced renal dysfunction (an increase in serum creatinine greater than or equal to 1.0 mg/dL) occurred in two (2%) patients in Group I and in six (21%) patients in Group II (p less than 0.001). Of the 48 patients with concomitant diabetes mellitus, the contrast limit was surpassed in 16, six (38%) of whom had contrast nephropathy. Only two of the 32 (6%) diabetic patients in whom the contrast limit was not exceeded had contrast nephropathy (p less than 0.001). CONCLUSIONS: Thus, contrast-induced renal dysfunction occurs infrequently if the amount of contrast material is limited in accordance with the degree of azotemia. Diabetic patients have a high incidence of contrast nephropathy, particularly when they receive an excessive amount of contrast. In patients with diabetes and renal impairment, it may be preferable to perform angiography as a staged procedure or to utilize alternative (non-contrast) techniques to obtain the desired information rather than to exceed the prescribed contrast limit.

Underestimation of cardiac output by thermodilution in patients with tricuspid regurgitation.

INTRODUCTION: This study was done to assess the accuracy and reliability of the thermodilution technique in measuring cardiac output in patients with tricuspid regurgitation. PATIENTS AND METHODS: In 30 subjects (17 men, 13 women, aged 50 +/- 14 [mean +/- SD] years), cardiac output was measured in close temporal proximity by thermodilution as well as Fick or indocyanine green dye, after which the presence and severity of tricuspid regurgitation were assessed by contrast right ventriculography or pulsed Doppler echocardiography. RESULTS: In the 13 patients without tricuspid regurgitation, there was excellent agreement between the results of thermodilution and Fick or indocyanine green dye cardiac output determinations (4.95 +/- 1.19 liters/minute by thermodilution, 4.90 +/- 1.11 liters/minute by Fick or indocyanine green dye; NS). In contrast, in the 17 patients with tricuspid regurgitation, the results of thermodilution were consistently lower than those of Fick or indocyanine green dye (4.22 +/- 1.45 liters/minute by thermodilution, 4.99 +/- 1.67 liters/minute by Fick or indocyanine green dye; p less than 0.001). CONCLUSION: Thus, the thermodilution technique of measuring cardiac output is inaccurate in patients with tricuspid regurgitation, yielding results that are consistently lower than the actual outputs.

Diagnostic and prognostic utility of right-sided catheterization and endomyocardial biopsy in idiopathic dilated cardiomyopathy.

To determine the value of cardiac catheterization and endomyocardial biopsy in patients with heart failure and dilated cardiomyopathy, the records of 61 patients (36 men, 25 women, ages 13 to 65 years) with this disorder were reviewed. Myocardial lymphocytic infiltration was present in 8 (13%). Three had myocyte degeneration and necrosis ("definite" myocarditis), whereas the other 5 had no degeneration or necrosis ("equivocal" myocarditis). Compared with the 53 without lymphocytic infiltration, these 8 patients more often had symptoms of a preceding viral illness (88 vs 30%, p = 0.002) and had a shorter duration of cardiac symptoms (18 +/- 18 vs 109 +/- 132 days [mean +/- standard deviation], p less than 0.001). Histologic features of the biopsy did not relate to survival, but right- and left-sided intracardiac pressures were higher (p less than 0.05) in nonsurvivors. Thus, (1) endomyocardial biopsy is most likely to show lymphocytic infiltration in patients with symptoms of a preceding viral illness and a short duration of cardiac symptoms, and (2) right- and left-sided hemodynamic variables at the time of biopsy may offer insight into prognosis.

Use of pulmonary capillary wedge pressure to assess severity of mitral stenosis: is true left atrial pressure needed in this condition?

There is disagreement concerning the use of the pulmonary capillary wedge pressure (in place of left atrial pressure) in assessing the presence and severity of mitral valve disease. This study was done to assess the accuracy and reliability of an oximetrically confirmed pulmonary capillary wedge pressure in measuring the transvalvular pressure gradient and valve area in patients with mitral stenosis. In 10 patients with mitral stenosis (1 man and 9 women; mean age +/- SD 47 +/- 7 years), pulmonary capillary wedge pressure was measured through an 8F Goodale-Lubin catheter with its wedge position confirmed by oximetry (oxygen saturation greater than or equal to 95%). In addition, a transseptal left atrial pressure was measured through a Brockenbrough catheter and left ventricular pressure was measured through a pigtail catheter. The mean and phasic left atrial and pulmonary capillary wedge pressures were similar (mean left atrial pressure 18 +/- 6 mm Hg; mean pulmonary capillary wedge pressure 18 +/- 8 mm Hg; p = NS). When the pulmonary capillary wedge pressure was used without adjustment for time delay, the transvalvular pressure gradient (9.8 +/- 3.3 mm Hg) and valve area (1.5 +/- 0.5 cm2) were significantly different (p less than 0.05) from the values obtained with use of left atrial pressure (7.2 +/- 2.9 mm Hg and 1.7 +/- 0.6 cm2, respectively). In contrast, when the pulmonary capillary wedge pressure was adjusted for the time delay through the pulmonary vasculature, the difference in gradients averaged only 1.7 mm Hg and the mitral valve areas were similar.(ABSTRACT TRUNCATED AT 250 WORDS)