Biomedical subjects
Publications and source records attributed to R H Peter.
This report describes a patient who presented with congestive heart failure secondary to a mitral annular-left atrial fistula. There was a remote history of Staphylococcus aureus endocarditis involving the mitral valve which was treated medically 30 years previously. The sterile fistula was managed surgically with an annuloplasty.
OBJECTIVES: The purpose of this study was to further explore the procedural safety of prolonged (15-min) dilation using an autoperfusion coronary angioplasty balloon by assessing the degree of myocardial damage or hemolysis, if any, occurring as a result of the procedure. BACKGROUND: Prolonged balloon inflation periods may be beneficial during percutaneous transluminal coronary angioplasty. The duration of standard balloon angioplasty is often limited by the occurrence of myocardial ischemia due to loss of anterograde blood flow. Autoperfusion angioplasty allows continued myocardial perfusion during balloon inflation and has previously been shown to reduce but not totally eliminate acute myocardial ischemia during prolonged (up to 15 min) balloon inflation. The risk of intravascular hemolysis as a result of autoperfusion angioplasty has not yet been fully delineated. METHODS: Sixty-two consecutive patients (76% men; mean age 58 years) undergoing elective percutaneous transluminal coronary angioplasty of a single lesion were studied. Serial electrocardiographic and creatine kinase MB isoenzyme data were examined to detect evidence of myocardial damage. Tests for hemolysis (plasma free hemoglobin, serum haptoglobin and serum lactate dehydrogenase) were obtained in the 1st 24 consecutive patients. RESULTS: Inflation time was 14 +/- 4 min (mean +/- SD) and the procedure was successful (less than or equal to 50% residual lesion stenosis) in 59 patients (95%). Electrocardiographic evidence of myocardial infarction (greater than 1 mm persistent ST segment depression, greater than 1 mm ST segment elevation or new Q waves) was not observed in any patient. Cardiac enzyme assays were within the normal range in all patients. No evidence of hemolysis was found in the 24 consecutive patients studied. CONCLUSIONS: We conclude that prolonged autoperfusion angioplasty can be performed in patients without clinical evidence of myocardial damage or hemolysis.
The feasibility and applicability of intravascular ultrasound (IVUS) of the coronary arteries were evaluated in 65 patients undergoing 70 coronary interventional procedures. Morphologic and quantitative analyses were performed with a mechanically rotated IVUS catheter (4.8Fr, 20 MHz) and with orthogonal view cineangiography. A semiautomated edge-detection algorithm was used for cineangiographic quantification. Coronary interventions included 45 percutaneous transluminal coronary angioplasties, 9 excimer lasers, 11 directional coronary atherectomies, 3 rotational atherectomies and 2 stents. Most lesions consisted of a mixture of plaque composition (hard, n = 30; soft, n = 64). Other unique morphologic data by IVUS were plaque topography (eccentric, n = 34; concentric, n = 36) and vessel dissection (IVUS [n = 29] versus angiography [n = 14], p less than 0.05). Postprocedure minimal lumen diameter and cross-sectional area measured by IVUS were larger and poorly correlated with angiography (r = 0.28, standard error of the estimate = 0.52 mm; r = 0.08, standard error of the estimate = 1.0 cm2, respectively). IVUS is more sensitive than angiography when assessing postintervention lesion characteristics including vessel dissection and plaque morphology. Catheter-based ultrasound appears to be a useful adjunct to contrast angiography when evaluating and comparing the therapeutic impact of conventional percutaneous transluminal coronary angioplasty with new technologies.
Historically, electrocardiographic criteria for right ventricular (RV) hypertrophy has achieved high specificity but low sensitivity. Recently, however, Butler-Leggett et al. have introduced three criteria that attained a 66% sensitivity in a population with RV hypertrophy due to mitral stenosis while maintaining a 95% specificity in an extensive normal control group. Electrocardiographic diagnosis of RV hypertrophy is principally dependent on changes in the QRS complex that may be masked or mimicked by myocardial infarction (MI). This dilemma has been confirmed by documentation of the low specificity of both the Selvester QRS scoring system for MI size estimation (greater than 3 points) and its screening subset (greater than 0 points) in a pure mitral stenosis population. This study introduces the population characterized by RV hypertrophy due to cor pulmonale, which has a mean pulmonary arterial systolic pressure that is higher than the mean for the mitral stenosis population and consequently suggests more severe RV hypertrophy. When compared, the Butler-Leggett criteria for RV hypertrophy are more sensitive in the new population than in the mitral stenosis population (89% versus 60%) and the Selvester QRS scoring system is less specific (12% versus 60%). Three sequential steps are suggested for electrocardiographic analysis: (1) diagnosis of RV hypertrophy using the Butler-Leggett criteria, (2) diagnosis of MI using the Selvester screening criteria in those patients with step 1 negative, and (3) estimation of MI size using the complete Selvester scoring system in patients with step 1 negative and step 2 positive.
The late restenosis rate after emergent percutaneous transluminal coronary angioplasty for acute myocardial infarction was assessed by performing outpatient follow-up cardiac catheterization in 79 (87%) of 91 consecutive patients who had been discharged from the hospital with a successful coronary angioplasty. The majority of patients (90%) received high dose intravenous thrombolytic therapy with streptokinase in addition to angioplasty. Similar follow-up data were obtained in 206 (90%) of 228 consecutive patients who had successful elective angioplasty during the same period. The interval from angioplasty to follow-up was 28 +/- 9 weeks for the myocardial infarction group and 30 +/- 11 weeks for the elective group. Baseline clinical variables were similar for both the myocardial infarction and elective groups except for a higher percentage of men in the infarction group (81 versus 63%, p = 0.001). The number of coronary lesions undergoing angioplasty and the incidence of intimal dissection were similar, but multivessel angioplasty was more common in the elective group (13 versus 4%, p = 0.02). The rate of in-hospital reocclusion was higher in the patients receiving angioplasty for myocardial infarction (13 versus 2%, p = 0.0001). At the time of late follow-up after hospital discharge, the patients with myocardial infarction were more often asymptomatic (79 versus 55%, p = 0.0001), and the rate of angiographic coronary restenosis was lower for the infarction group both overall (19 versus 35%, p = 0.006) and when multivessel angioplasty patients were excluded (19 versus 33%, p = 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
An autoperfusion balloon catheter was developed to allow passive myocardial perfusion during inflation through a central lumen and multiple side holes in the shaft proximal and distal to the balloon. We report its safety and efficacy in 11 patients undergoing elective angioplasty to a single coronary lesion. Each lesion was dilated three times with the autoperfusion inflation bracketed between two inflations by standard angioplasty catheters. Chest pain score, 12-lead electrocardiogram, heart rate, and mean aortic pressure were recorded before each inflation and at 1-minute intervals after inflation. Inflation duration during autoperfusion angioplasty (513 +/- 303 seconds) was longer than for the pre- (107 +/- 55 seconds, p = 0.0004) and post- (139 +/- 71 seconds, p = 0.0006) standard dilatations. The maximum ST-segment elevation and depression in any lead during autoperfusion angioplasty (0.3 +/- 0.5 and 0.6 +/- 0.8 mm) was significantly less than for the pre- (2.4 +/- 1.7 mm, p = 0.002 and 2.2 +/- 1.3 mm, p = 0.0004) or post- (1.9 +/- 1.3 mm, p = 0.002 and 1.6 +/- 1.3 mm, p = 0.018) standard dilatations at the same point in time. Maximal chest pain score during autoperfusion (3.2 +/- 3.5) was lower than for the pre- (6.1 +/- 2.1, p = 0.003) but not the post- (5.2 +/- 3.1, p = 0.07) standard angioplasty. All 11 patients underwent successful, uncomplicated procedures. We conclude that this autoperfusion catheter significantly reduces ischemic symptoms and signs during coronary angioplasty, allowing prolonged periods of balloon inflation.
STUDY OBJECTIVE: To prospectively investigate the evidence for embolic phenomena associated with percutaneous mitral and aortic valvuloplasty. DESIGN: Prospective, consecutive case series before and after balloon valvuloplasty. SETTING: Referral center hospital and cardiac catheterization laboratory. PATIENTS: Consecutive sample of 32 patients having balloon valvuloplasty for critical symptomatic stenosis of the mitral or aortic valve. Twenty-six patients had aortic stenosis; 6 had mitral stenosis. INTERVENTION: Computed tomography of the head, funduscopy, and electrocardiography were done in all patients before and after valvuloplasty. Cardiac isoenzymes were measured serially in 19 patients. MEASUREMENTS AND MAIN RESULTS: Previous cerebral infarction was seen in nine patients, with three showing a new abnormality after aortic valvuloplasty. In one of these patients a funduscopic hemorrhage was detected by photography. Total creatinine kinase and MB fraction were elevated in 1 of 19 patients. Serial electrocardiograms were unchanged in all patients. CONCLUSIONS: The incidence of cerebral neurologic events and myocardial injury are acceptably low after balloon valvuloplasty of calcific aortic and mitral stenosis. Both episodes of symptomatic cerebral infarction occurred in patients with apparent bicuspid aortic valvular stenosis, suggesting that calcific bicuspid aortic stenosis may be associated with more neurologic events after aortic valvuloplasty.
We have described a young man who had acute myocardial infarction after his first use of cocaine. This case demonstrates that potentially lethal myocardial infarctions may be associated with such initial "experimentation" with cocaine even in relatively small doses. Cocaine intoxication should be considered in young patients with acute myocardial ischemia or necrosis. We recommend that cocaine metabolites be checked in the urine if a drug history is unreliable in such patients.
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Right ventricular infarction is usually associated with coronary artery disease and concomitant left ventricular infarction. Isolated right ventricular subendocardial necrosis was discovered at autopsy in a 52-year-old woman with pulmonary hypertension, right ventricular hypertrophy, and normal coronary arteries, who died with septicemia 41 days after mitral valve replacement. This represents the first well-documented report of isolated right ventricular subendocardial infarction associated with normal coronary arteries.
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An undated Cordis Ducor polyurethane coronary catheter fractured and separated in the aortic arch during a cardiac catheterization, and was removed with an intravascular retriever. The recovered specimen appeared brittle, prompting an investigation of the effects of aging on the tensile strength of 91 polyurethane catheters manufactured by Cordis and the United States Catheter and Instrument Company (USCI). Cordis catheters have stable tensile strength for five years from manufacture, but then deteriorate substantially by seven years, particularly at the bond between the catheter tip and the stainless steel-reinforced catheter body. The deterioration is associated with the microscopic appearance of deep cracks in the catheter lumen wall. USCI catheters showed a modest but significant loss of tensile strength by three years after manufacture at the catheter bond. It would seem prudent to place a three-year expiration date on USCI polyurethane catheters, similar to those already on Cordis catheters.
We analyzed the clinical outcomes in 688 patients with isolated stenosis of one major coronary artery. The survival rate among patients with disease of the right coronary artery (RCA) was higher than that among patients with left anterior descending (LAD) or left circumflex coronary artery (LCA) disease. The survival rate among patients in all three anatomic subgroups exceeded 90% at 5 years. The presence of a lesion proximal to the first septal perforator of the LAD was associated with decreased survival compared with the presence of a more distal lesion. For the entire group of one-vessel disease patients, total ischemic events (death and nonfatal infarction) occurred at similar rates regardless of the anatomic location of the lesion. Left ventricular ejection fraction was the baseline descriptor most strongly associated with survival, and the characteristics of the angina had the strongest relationship with nonfatal myocardial infarction. No differences in survival or total cardiac event rates were found with surgical or nonsurgical therapy. The relief of angina was superior with surgical therapy, although the majority of nonsurgically treated patients had significant relief of angina. The survival rate of patients with one-vessel coronary disease is excellent, and the risk of nonfatal infarction is low. Clinical strategies for the care of these patients must consider the long-term clinical course of one-vessel coronary disease.
The effect of reperfusion on regional left ventricular performance following acute myocardial infarction in man was determined. Intracoronary streptokinase was administered in 24 patients within 6 h of the onset of symptoms. 15 patients (62%) were successfully recanalized during the initial study. Mean percent radial shortening (%RS) in both the jeopardized and compensatory regions were determined using 23 radii from the centroid of diastolic and systolic angiographic silhouettes. Sequential measurements were obtained during repeat cardiac catheterization studies at 24 h in 19 patients and before discharge from the hospital (16 +/- 11 d) in 15 patients. At the time of the predischarge study, each acutely reperfused patient showed improvement in %RS in the jeopardized region (P = 0.01) with 56% returning to the normal range. Despite the uniform improvement in the contractile function of the jeopardized region in each reperfused patient, the global ejection fraction showed no improvement or a decrease at the time of the chronic study in 44%. This was due to a decrease in the compensatory wall motion in the uninvolved segments between the acute and chronic study in each case. Neither the %RS nor the ejection fraction changed significantly at the time of the chronic study in the patients who could not be acutely recanalized. These data indicate (a) significant salvage of jeopardized myocardium associated with recovery of contractile function in patients reperfused during the first 6 h of chest pain following acute myocardial infarction; (b) no improvement in regional or global left ventricular performance in patients who could not be reperfused acutely; and (c) the ejection fraction is strongly influenced by changes in the compensatory wall motion of the uninvolved segments and does not accurately reflect changes in the contractile function of the jeopardized myocardium.
An increasing number of people who have undergone surgical repair of tetralogy of Fallot are living long lives. Several late sequelae of corrected tetralogy of Fallot have been found, including residual ventricular septal defect, restenosis of the pulmonary outflow tract, ventricular tachycardia, and right ventricular failure from pulmonary insufficiency. A long-term survivor of corrected tetralogy of Fallot is reported with acquired coronary artery disease unrelated to the congenital anomaly or its correction as an additional cause of late morbidity in this select but growing population of patients.
Hydralazine reduces pulmonary vascular resistance in patients with primary and secondary pulmonary hypertension, but the effects on right ventricular function of a change in resistance without a reduction in pulmonary arterial pressure are not known. We evaluated the hemodynamic effects of hydralazine, 50 mg, administered orally every 6 hours for 48 hours in 14 patients with right ventricular failure and pulmonary hypertension resulting from various causes. Hydralazine reduced mean right ventricular end-diastolic pressure from 17.4 +/- 5.6 to 11.6 +/- 5.3 mm Hg (p less than 0.001) and increased cardiac output and stroke volume by more than 40%. In nine patients who had no change in mean pulmonary arterial pressure after hydralazine, total pulmonary resistance decreased from 15.9 +/- 6.0 to 10.6 +/- 4.3 (p less than 0.001) and cardiac index increased from 2.07 +/- 0.51 to 2.97 +/- 0.91 (p less than 0.005). There was a close correlation between the reductions in total pulmonary resistance and right ventricular end-diastolic pressure (r = 0.73)). These data suggest that hydralazine can increase cardiac output and reduce right ventricular end-diastolic pressure even when pulmonary arterial pressure remains unchanged.