Citations

BACKGROUND Platelet-thrombus formation is a complication of arterial wall deep injury by balloon angioplasty that may lead to acute arterial occlusion and may contribute to restenosis. METHODS AND RESULTS Because common platelet-inhibitor drugs with a heparin bolus (100 units/kg) may be effective in inhibiting platelet-thrombus formation after arterial angioplasty, these were compared with a bolus of heparin alone (control), the specific thrombin inhibitor hirudin (1.0 mg/kg), and saline (hirudin control) in normal pigs after angioplasty of the common carotid arteries. In the presence of deep arterial wall injury (injury exposing the media), indium-111-labeled platelet deposition (x 10(6)/cm2) was 68.8 +/- 12.3 and 48.1 +/- 16.9 in the control animals. This was significantly reduced by pretreatment with low-dose aspirin (1 mg/kg/day), by high-dose aspirin (20 mg/kg/day) plus dipyridamole, and especially by thrombin inhibition with hirudin. Treatment regimens with aspirin alone (20 mg/kg/day), dipyridamole alone, or sulfinpyrazone were ineffective. Likewise, the incidence of mural thrombosis was 75% and 80% in deeply injured arteries of controls and was significantly reduced to 46% with aspirin plus dipyridamole, 25% with low-dose aspirin, and 0% with hirudin. The incidence of mural thrombosis was unchanged with high-dose aspirin (69%), dipyridamole (90%), or sulfinpyrazone (92%). This mural thrombosis could not be identified by angiography. In the presence of mild injury (deendothelialization), platelet deposition was low (less than 10 x 10(6)/cm2, a single layer) and was not changed by any therapy, including hirudin. CONCLUSIONS These therapies do not affect platelet adhesion to deeply or mildly injured artery. These data suggest a greater role for thrombin inhibition than with thromboxane or cyclooxygenase inhibition in the pathogenesis of platelet-rich mural thrombosis after deep injury during angioplasty. Antithrombotic therapy for arterial thrombosis by thrombin inhibition appears promising.

BACKGROUND Transient bacteremia may lead to endocarditis in patients with significant valvular lesions. METHODS AND RESULTS Because transesophageal echocardiography selects a patient population with a high prevalence of valvular lesions, we prospectively evaluated the risk of transient bacteremia associated with transesophageal echocardiography in 49 patients. Blood cultures were obtained immediately before transesophageal echocardiography and at 5, 10, and 20 minutes after the start of the procedure. For each culture, 30 ml venous blood was obtained and 10 ml was inoculated into each of an Isolator tube, Septi-chek bottle, and a nonvented Trypticase soy broth bottle. Broth cultures were incubated for 14 days. Blood from the Isolator tube was plated onto appropriate media for recovery of bacteria and fungi. Two patients were excluded from analysis because the final two sets of blood cultures could not be obtained. Among the remaining 47 study patients, two preprocedure control blood cultures were positive, and two of 141 subsequent cultures were positive. All isolates were considered contaminants. Thus, we found no significant bacteremia due to pathogenic oral flora during transesophageal echocardiography (0%; 95% CI, 0.0-7.5%). CONCLUSIONS Although recommendations for antimicrobial prophylaxis for transesophageal echocardiography should be individualized for each patient, many patients may not require antimicrobial prophylaxis.

BACKGROUND Transthoracic Doppler echocardiography examination has become an integral part of the investigations performed in patients with mitral valve prostheses. The limitations of the transthoracic approach are well documented. Transesophageal echocardiography provides a unique window for achieving a clear view of the mitral prosthesis. METHODS AND RESULTS This study shows the usefulness of transesophageal echocardiography in clinical practice for assessment of patients with a mitral valve prosthesis. This technique demonstrated an abnormality in 48% of patients who had normal results on transthoracic examination. The overall sensitivity of transesophageal echocardiography was 96%. CONCLUSIONS Transesophageal echocardiography constitutes an essential part of a comprehensive two-dimensional/Doppler echocardiographic examination in patients with suspected malfunction of mitral prostheses.

BACKGROUND Endothelin is an endothelium-derived peptide that produces sustained contraction of arterial and venous smooth muscle in vitro. Several studies have established endothelin as a systemic, renal, and coronary vasoconstrictor in vivo at pharmacological concentrations. Such concentrations of endothelin were antinatriuretic in association with activation of the renin-angiotensin-aldosterone system. Recent studies have demonstrated that endothelin is present in the plasma and that its plasma concentrations are increased in various pathological states associated with systemic and renal vasoconstriction. To date, it remains unclear if such increases in circulating endothelin are associated with biological activity. Thus, the objective of this study was to determine the biological action of endothelin on cardiorenal and endocrine function through administration of exogenous endothelin, which achieves plasma concentrations that have been reported in various pathophysiological conditions. METHODS AND RESULTS Experiments were conducted in two groups of anesthetized dogs. In group 1, endothelin-1 was infused intravenously at 2.5 ng/kg/ml (n = 6), which produced a doubling of circulating concentrations. Group 2 (n = 8) received saline vehicle to serve as a time control. The current studies demonstrate that a twofold increase in plasma endothelin concentrations did not affect mean blood pressure or coronary blood flow. Heart rate and cardiac output decreased in association with increased renal and systemic vascular resistances and antinatriuresis. CONCLUSIONS The present studies demonstrate that endothelin at pathophysiological plasma concentrations produced by exogenous endothelin has biological action. These studies support a functional role for endogenous endothelin as a potentially pathophysiological vasoconstrictor peptide hormone in the regulation of cardiovascular, renal, and endocrine function.

BACKGROUND Patients who have chest pain without electrocardiographic ST elevation are not candidates for thrombolytic therapy in most clinical trials. This study examined the value of technetium-99m-Sestamibi tomographic imaging to assess myocardial perfusion in patients during chest pain without ST elevation. METHODS AND RESULTS Tc-99m-Sestamibi was injected in 14 patients who had chest pain without ST elevation, who subsequently developed enzymatic evidence of myocardial infarction within 24 hours. Tomographic imaging was performed 1-6 hours after injection. Thirteen of 14 patients showed significant perfusion defects indicative of acute myocardial infarction consistent with absent perfusion (20 +/- 15% of the left ventricle; range, 2-53%); one patient had normal images. Because of the absence of definitive electrocardiographic changes, only five patients received reperfusion therapy within 6 hours of the onset of chest pain. Regional wall motion abnormalities were present in nine of nine patients undergoing contrast ventriculography and correlated with the location of the Tc-99m-Sestamibi perfusion defect. At the time of subsequent coronary angiography, total arterial occlusion was present in 11 of the 14 patients. The infarct-related artery could be identified in 13 of the 14 patients. In six of these 13 patients, the left circumflex was the infarct-related artery. CONCLUSIONS Patients who have chest pain without electrocardiographic ST elevation may have arterial occlusion and significant myocardium at risk. Tc-99m-Sestamibi imaging may be of benefit in identifying these patients early so that they can be considered for acute reperfusion therapy.

BACKGROUND We have previously characterized the left ventricular diastolic filling abnormalities in cardiac amyloidosis by Doppler methods. The various filling patterns were shown to be related to the degree of cardiac amyloid infiltration. The purpose of this study was to determine the value of Doppler diastolic filling variables for assessing prognosis in cardiac amyloidosis. METHODS AND RESULTS We performed pulsed-wave Doppler studies of the left ventricular inflow and obtained clinical follow-up data in 63 consecutive patients with biopsy-proven systemic amyloidosis. All patients had typical echocardiographic features of cardiac involvement. The patients were subdivided into two groups according to deceleration time: Group 1 (33 patients) had a deceleration time of 150 msec or less, indicative of restrictive physiology, and group 2 (30 patients) had a deceleration time of more than 150 msec. Of the 63 patients, 32 (51%) died during a mean follow-up period of 18 +/- 12 months. Of these deaths, 25 (78%) were cardiac deaths, and 19 of the 25 patients (76%) were from group 1. The 1-year probability of survival in group 1 was significantly less than that in group 2 (49% versus 92%, p less than 0.001). Bivariate analysis revealed that the combination of the Doppler variables of shortened deceleration time and increased early diastolic filling velocity to atrial filling velocity ratio were stronger predictors of cardiac death than were the two-dimensional echocardiographic variables of mean left ventricular wall thickness and fractional shortening. CONCLUSIONS Doppler-derived left ventricular diastolic filling variables are important predictors of survival in cardiac amyloidosis.

The use of roentgen videometry as a means of studying regional left ventricular wall dynamics and performance was evaluated in 32 patients undergoing coronary arteriography. Nine patients had normal coronary arteriograms and hemodynamic findings (group 1), 8 patients had generalized decrease in left ventricular contraction and abnormal hemodynamic findings (group 2), and 15 patients with coronary artery disease had regional wall dynamics abnormalities (group 3). Sixty-per-second determinations of wall thickness were performed in selected sites of the left ventricle. Measurements performed included end-diastolic wall thickness (EDTw), mean and peak rates of systolic wall thickening (m and p dTw/dt), and fractional systolic increase in wall thickness (ΔTw/EDTw). In patients with uniformly performing ventricles (groups 1 and 2), these parameters correlated well with other parameters of ventricular function. Best distinction between the "normal" group (group 1) and the "abnormal" group (group 2) was achieved when the rates of thickening (m and p dTw/dt) were utilized ( P < 0.001). In patients of group 3, three types of abnormal regional wall dynamics could be determined and quantified objectively: hypokinesia (decreased p dTw/dt), akinesia (p dTw/dt = 0), and dyskinesia (p dTw/dt < 0). The severity of the abnormality of the wall dynamics correlated well with the presence or absence of a previous infarction on the electrocardiogram, and the anatomic location was strongly correlated with the distribution and severity of coronary artery lesions within a given ventricle.

Two patients with corrected transposition of the great arteries and ventricular rotation are described. The ventricular rotations encountered were about the longitudinal and the anteroposterior axes, respectively. The ventricular rotation affected the plane of the ventricular septum, the inflow and outflow tracts of the ventricles, and the interrelationship of the great arteries. Surgical closure of an associated ventricular septal defect was not without its problems.

Twenty-two patients had ventricular septal rupture complicating acute myocardial infarction. Sixteen of the 22 patients underwent surgical repair. The clinical findings, catheterization data, and operative results suggest that closure of the rupture should be delayed when possible from three to six weeks after the infarction to allow firm fibrous healing of the region. When surgery is thus delayed, the operative risks are smaller and the long-term results are good.