Collaborative clinical laboratory evaluation of an individual MIC strip system.

Susceptibility results obtained with individualized MIC strips (MICRO-MIC) agreed with the standard microdilution broth method at a level of 96% or greater for each of the 10 antimicrobial agents tested.

Constrictive pericarditis: a case requiring pericardiectomy following Dressler's postmyocardial infarction syndrome.

Exertional neck tightness developed 6 months following a myocardial infarction that was complicated by Dressler's syndrome. The patient's symptoms were initially interpreted as angina pectoris but did not respond to antianginal therapy. Findings at cardiac catheterization were indicative of constructive pericarditis. The diagnosis was confirmed at pericardiectomy and the symptoms resolved completely postoperatively. Constrictive pericarditis should be considered as an unusual but important sequel of Dressler's postmyocardial infarction syndrome.

Salvage of acutely ischemic myocardium by emergency coronary artery bypass grafting.

After cardiac catheterization a 53-year old patient developed widespread myocardial ischemia that produced electromechanical dissociation and cardiogenic shock. The administration of methylprednisolone, the initiation of cardiopulmonary bypass and hypothermia within 40 min of the onset of ischemia, and reperfusion within 90 min of the onset of ischemia were sufficient to salvage a major portion of the ischemic myocardium.

Hemodynamic effects of positive-pressure inflation.

In 14 anesthetized mongrel dogs, we studied the factors that influenced aortic systolic pressure (PaO) and peak aortic systolic flow (Qao) during positive-pressure inflations at three respiratory rates: 8, 14, and 24 breaths/min. At all three respiratory rates, pulmonary arterial flow fell by 15% of the preinspiratory value by end inhalation. Qao also fell at all three respiratory rates, reaching a nadir close to end exhalation (EE). Qao fell less (7% of the base line) at the fast respiratory rate than at the medium and slow respiratory rates (15% of the base line). Pao rose more during the early part of inflation at the medium and fast rates (5 +/- 0.9 Torr) than at the slow rate (3 +/- 0.7 Torr); then Pao fell to a nadir near EE at the slow (-5.6 +/- 1.6 Torr) and at the medium (-2.3 +/- 1 Torr) respiratory rates. At the fast rate it fell to a value not different from control (0.1 +/- 0.5 Torr). The ratio of peak arterial pressure to peak arterial flow increased throughout inflation reaching a peak at EE. A model was developed that predicted the major qualitative features of the changes in Qao seen in these studies. Changes in Pao resulted from the interaction between decreases in Qao and transmitted increases in pleural pressure, and are modified by changes in systemic impedance.

Left ventricular function after repair of tetralogy of fallot and its relationship to age at surgery.

Left ventricular (LV) work-function curves were used to assess LV performance in eight postoperative tetralogy of Fallot (TOF) patients who underwent repair before 2 years of age (group 1) and 12 patients who underwent repair after 2 years of age (group 2). All patients were without significant residual shunts or pulmonary stenosis. Results were compared with those in seven control patients. Left- and right-heart hemodynamics were measured at various levels of afterload induced by methoxamine while heart rate was maintained constant. Cardiac output was serially measured. The slope (m) for each patient's LV end-diastolic pressure (EDP) vs LV minute-work index (MWI) relationship was determined. There were no significant differences in resting cardiac index, LV systolic pressure, LVEDP, aortic oxygen saturation or MWI among the groups. However, with afterload stress, group 2 patients had abnormal work-function curves with depressed slopes (m = 0.21 +/- 0.04) compared with the values for group 1 patients (m = 0.89 +/- 0.13, p less than 0.001) or the control group (m = 1.13 +/- 0.12, p less than 0.001). Thus, LV dysfunction unmasked by an afterload stress was present in the older TOF patients but not in the patients repaired during infancy. These findings raise the possibility that early, definitive repair of TOF may help preserve postoperative LV function.

Hemodynamic effects of nitrous oxide administered during cardiac catheterization.

To assess the effects of nitrous oxide on hemodynamics and left ventricular function in man, 30 patients (24 of whom had coronary artery disease) were studied at the time of cardiac catheterization. Left ventricular peak-systolic pressure and end-diastolic volume showed no significant change during nitrous oxide inhalation. The maximum rate of pressure rise declined slightly, but left ventricular end-diastolic pressure and ejection fraction were unchanged. Heart rate and cardiac index declined modestly. The pressure-rate product and left ventricular minute work index decreased, suggesting a decline in myocardial oxygen requirements. These data suggest that nitrous oxide inhalation does not produce important depression of left ventricular performance. The consistent decrease in the determinants of myocardial oxygen demand suggests that use of this analgesic agent may be helpful in patients with coronary heart disease.

Platelet activation during exercise-induced myocardial ischemia.

Because platelet activation may be important in the worsening of coronary atherosclerosis, we used a radioimmunoassay for platelet factor 4 to study platelet behavior in patients with coronary-artery disease. Forty patients had paired blood samples withdrawn for measurement of the plasma level of platelet factor 4 before and after a standardized exercise-tolerance test. Twenty patients had positive tests, and 19 of those 20 had clinical or angiographic evidence of coronary-artery disease. Eleven of the 20 had a greater than 50 per cent increase in platelet factor 4 after exercise. The remaining nine had positive exercise tests without rises in platelet factor 4. Elevated levels returned to normal within 15 minutes of exercise. Eighteen of 20 patients with negative exercise tests had no rise in platelet factor 4 after exercise. We conclude that a subset of patients with coronary-artery disease and exercise-induced myocardial ischemia had evidence of platelet activation and secretion. (N Engl J Med 302:193-197, 1980).

Right ventricular diastolic pressure in coronary artery disease.

Right ventricular hemodynamics were evaluated in 179 patients with coronary artery disease to determine the effects of chronic ischemia on right ventricular diastolic pressure. Abnormal right ventricular filling pressures occurred only in patients with an abnormal right ventricular systolic pressure or an abnormal left ventricular end-diastolic pressure. Of the 63 patients whose right ventricle was stressed by an increased systolic load secondary to passive pulmonary hypertension, 44 (72 percent) had an abnormal right ventricular end-diastolic pressure. In this group obstruction of vessels serving the right ventricular free wall or septum, or both, was almost universal (43 of 44, 98 percent) and a significantly increased incidence of inferior infarction (P less than 0.05) was noted. Such obstruction was significantly less frequent in patients with normal filling pressures (10 of 17, 59 percent; P less than 0.001). Compared with patients with coronary artery disease, patients with passive pulmonary hypertension due to aortic stenosis or mitral stenosis had significantly greater degrees of pulmonary hypertension (P less than 0.05) yet slightly lesser elevations of right ventricular end-diastolic pressure. These data suggest that in patients with ischemic heart disease the right ventricle exhibits diastolic dysfunction at lower levels of afterload stress than it would with normal coronary blood flow.

Effects of normal and loaded spontaneous inspiration on cardiovascular function.

To assess the hemodynamic effects of spontaneous inspiration, we studied 12 anesthetized mongrel dogs during normal and loaded inspiration, before and after bilateral cervical vagotomy. Peak aortic flow fell (15--20%) whereas peak pulmonary artery flow rose (15--20%) under all conditions. When aortic flow fell, left ventricular diastolic size decreased whereas aortic and left atrial transmural pressures increased slightly. Right ventricular diastolic size and right atrial transmural pressure increased. During inspiratory loading transmural pressures rose more, but the fall in aortic flow remained the same. After vagotomy, inspiration was prolonged, allowing aortic flow to return to preinspiratory levels. At this time left ventricular diastolic size was increased compared to preinspiratory levels and there were further increases in left atrial and aortic transmural pressures. We have concluded that at least two factors affect aortic flow during inspiration: 1) a decrease in left ventricular preload that is associated with decreased left ventricular compliance, and 2) increased impedance to left ventricular emptying as reflected by the increase in aortic transmural pressure. This may play a greater role during inspiratory loading and when inspiration is prolonged.

Physiologic determinants of the electrocardiographic diagnosis of left ventricular hypertrophy.

The relative importance of left ventricular (LV) geometry, wall thickness, and mass on the inscription of left ventricular hypertrophy (LVH) on the ECG was examined in 93 patients; 36 had no LVH on the ECG, 10 had borderline voltage for LVH, and 47 had LVH on the ECG. LV cineangiograms in the right anterior oblique projection were analyzed for LV end-diastolic volume, free wall thickness (h), semiminor radius (R), LV mass index (LVMI), and the geometric relations described by h/R, mass/volume, and h . R. Although mean LVMI was greater in patients whose ECG voltage was either borderline or diagnostic of LVH, increased LVMI also occurred without LVH on the ECG. None of the variables (h, R, h/R or mass/volume) reliably indicated when LVH would be inscribed on the ECG. The product of h . R, however, defined three electrocardiographic groups; all patients with LVH on their ECG had h . R greater than 2.6 cm2. Wall thickening sufficient to result in an increased LV mass did not result in LVH on the ECG unless sufficient concurrent chamber dilatation was present. Thus, a critical geometric relationship resulting from the interplay of wall thickness and chamber dilatation is necessary for LVH to appear on the ECG. This finding is consistent with the solid-angle theory of electrocardiography as it relates to ventricular hypertrophy.

Coronary hemodynamic and myocardial metabolic alterations accompanying coronary spasm.

Arterial pressure, coronary sinus blood flow with the thermodilution technique and calculated coronary vascular resistance were measured and coronary arteriography performed at rest and after the administration of ergonovine in 14 patients with atypical chest pain (group 1) and 6 patients with variant angina (group II). Mild diffuse narrowing of the left coronary bed in group I was not accompanied by S-T segment shifts, and coronary vascular resistance did not change significantly. In contrast, severe focal spasm (greater than 90 percent narrowing) of the left anterior descending coronary artery in group II patients was accompanied by S-T elevation and a marked overall increase in coronary vascular resistance (from 0.65 +/- 0.07 to 1.14 +/- 0.10 mm Hg/ml per min) (P less than 0.005). In addition, the myocardial arteriovenous oxygen difference increased and net lactate extraction changed to lactate production in the two patients in group II in whom these measurements were made. Thus, thermodilution coronary sinus blood flow measurement may be a sensitive method for detecting primary increases in coronary vascular resistance due to a high grade focal spasm in the left anterior descending coronary artery.

Left heart catheterization and angiography via the percutaneous femoral approach using an arterial sheath.

An arterial sheath with a proximal hemostasis valve and a side-arm extension tube was used in 562 consecutive patients undergoing cardiac catheterization and angiography via the femoral approach. Serious complications were rare. There was one death, one peripheral embolism, and one episode of delayed groin hemorrhage. The incidence of minor complications, including hematoma formation, in this series compares favorably with our own and the reported experience of others using the conventional percutaneous femoral approach. The sheath technique facilitated catheter exchanges and reduced patient discomfort. In addition, femoral artery pressure could be monitored via the side arm of the sheath during the catheterization. This proved helpful during retrograde catheterization of patients with aortic stenosis, as well as in detection of damping of coronary artery catheter tip pressure during coronary arteriography and hypotension following left ventriculography. Based upon this experience, use of an arterial sheath has become our standard practice when left heart catheterization is performed via the femoral approach, and the use of several different catheters is anticipated.

Effect of nitroprusside on regional myocardial blood flow in coronary artery disease. Results in 25 patients and comparison with nitroglycerin.

The effect of nitroprusside on regional myocardial specific blood flow (RMBF) was evaluated in 25 patients with the xenon-133 washout technique. Six patients were normal (group 1), six patients had coronary artery disease without collateral vessels (group 2), and thirteen patients had coronary artery disease with collateral vessels (group 3). In group 1, RMBF was unchanged following nitroprusside. RMBF decreased significantly in both group 2 and group 3, including seven patients in group 3 with high-grade collateral vessels. The results were compared to the effect of nitroglycerin in 31 patients previously studied using the same technique. Mean arterial pressure and pressure-rate product were comparably reduced by both drugs. In contrast to the findings with nitroprusside, after sublingual nitroglycerin RMBF decreased markedly in normals and increased in patients with coronary artery disease and high-grade collaterals. The data suggest that nitroprusside may primarily affect resistance vessels within the coronary circulation, as opposed to the effect of nitroglycerin on conductance vessels. Thus, nitroprusside could result in redistribution of blood flow away from ischemic areas and potentially increase ischemic injury in some patients with coronary artery disease.