Value and limitations of transesophageal echocardiography in evaluating prosthetic or bioprosthetic valve dysfunction.
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Adult↗
Biomedical subjects
R A O'Rourke
Publications and source records attributed to R A O'Rourke.
Systolic anterior motion of the chordal apparatus after mitral ring insertion.
To describe the Doppler and two-dimensional echocardiographic characteristics of systolic anterior motion of the chordal apparatus after mitral annuloplasty, 24 consecutive patients (19 men and 5 women; mean age, 55 years) were studied with the use of serial Doppler and two-dimensional echocardiography, which included preoperative transthoracic, intraoperative epicardial, and postoperative transthoracic examinations at 1 week after annuloplasty and every 3 months thereafter for up to 12 months. Systolic anterior leaflet motion of the mitral valve was not seen in this series; however, chordal systolic anterior motion was seen in three patients during surgery and in one additional patient at the time of the 1-week transthoracic examination. During subsequent studies at 3-month intervals, chordal systolic anterior motion was not present. The left ventricular outflow tract velocities were normal in all patients with and without chordal systolic anterior motion. In conclusion, chordal systolic anterior motion should be differentiated from leaflet systolic anterior motion after mitral annuloplasty because the former is a transient, benign, and relatively common finding.
Adult↗
Role of myocardial revascularization in sudden cardiac death.
Extensive atherosclerotic coronary artery disease is by far the most common pathological finding in patients with sudden cardiac death, and acute myocardial ischemia is often a contributing factor. Clinical trials using beta-blockers in postinfarction patients and bypass coronary artery surgery in patients with stable coronary artery disease have demonstrated a reduction in both sudden and total cardiac mortality after intervention. Information concerning the presence and extent of coronary artery disease, global and regional ventricular function, the presence or absence of ventricular aneurysms, and whether or not ischemia is inducible influences therapeutic management. Myocardial revascularization should be considered a primary therapy in patients with critical coronary artery stenosis, significant regions of myocardium at risk, and no inducible ventricular arrhythmias at electrophysiological testing. In patients with inducible polymorphic ventricular tachycardia or ventricular fibrillation, postoperative testing is essential, since only 50% will be suppressed by coronary artery surgery alone. In patients with inducible sustained monomorphic ventricular tachycardia and scars due to prior myocardial infarction, surgical revascularization alone will usually not be sufficient to prevent postoperative induction of the same arrhythmia. There are no data to support percutaneous transluminal coronary angioplasty as the sole therapy for post-sudden death patients who have inducible ventricular tachycardia or ventricular fibrillation on electrophysiological testing.
Angioplasty, Balloon, Coronary↗
Noninvasive and invasive testing after myocardial infarction.
Recurrent myocardial ischemia, moderate to marked depression of left ventricular systolic function, and late-occurring or recurrent cardiac arrhythmia indicate increased risk for patients with acute myocardial infarction. Some patients, on the basis of high risk and/or unsuccessful response, will be early candidates for early aggressive diagnostic and therapeutic procedures. Others will have clinical indicators of increased risk during hospitalization that warrant diagnostic coronary arteriographic assessment before discharge. Still other patients with low risk clinical characteristics can be further stratified by predischarge or early postdischarge stress testing for myocardial ischemia, left ventricular functional reserve, and/or likely occurrence of arrhythmias. Some stratified to low risk patients will be treated only with secondary prevention measures. Others at higher risk will undergo more aggressive evaluation and subsequent medical or surgical therapy.
Follow-Up Studies↗
Altered beta adrenergic receptor function in subjects with symptomatic mitral valve prolapse.
Individuals with mitral valve prolapse (MVP) frequently show symptoms of a hyperadrenergic state. beta adrenergic receptor characteristics were compared in the lymphocytes of subjects with symptomatic MVP and control subjects during rest and exercise. At rest, the proportion of receptors binding agonist with high affinity, as determined from isoproterenol competition for (-)[125I]-iodopindolol binding sites, was greater in MVP subjects than in controls. With exercise, the proportion of high-affinity receptors in MVP subjects decreased to control levels. Isoproterenol stimulation of lymphocyte 3',5'-cyclic adenosine monophosphate (cyclic AMP) also was greater in MVP subjects than in controls at rest, but not during exercise. Plasma catecholamine concentrations in MVP subjects were normal during both rest and exercise. Unlike exercise, isoproterenol infusion elicited clinical manifestations of increased adrenergic responsiveness in MVP subjects. The beta receptor in exercised MVP subjects exhibited unusually high affinity agonist binding (i.e. a lower dissociation constant KH than in either the same subjects at rest or exercised controls) and also abnormal coupling to the stimulatory guanine nucleotide-binding regulatory protein (GS) of adenylate cyclase, as reflected by the inability of guanine nucleotide to convert the receptor to a low-affinity state. These findings suggest that functional alteration of the beta adrenergic receptor, in the absence of abnormal plasma catecholamine levels, might contribute to the hyperadrenergic state of MVP subjects at rest. However, desensitization of high affinity beta receptors or altered receptor-GS coupling might preserve normal adrenergic responsiveness during exercise.
Adult↗
Risk stratification after myocardial infarction. Clinical overview.
Many patients with an acute myocardial infarction can be stratified into subgroups that are at high risk for morbidity and mortality on the basis of clinical characteristics that indicate recurrent myocardial ischemia, persistent left ventricular dysfunction, and/or recurrent cardiac arrhythmias. In patients with uncomplicated myocardial infarction the assessment of symptoms, physical findings, and ECG changes during predischarge exercise testing often identifies patients at increased risk for further cardiac events. Because of the suboptimum sensitivity and specificity of the exercise ECG for detecting myocardial ischemia, myocardial perfusion imaging with 201Tl and/or assessment of global and segmental ventricular function by two-dimensional echocardiography or radionuclide cineangiography during or immediately after exercise are often added to the predischarge risk stratification.
Arrhythmias, Cardiac↗
Demonstration of differential post-stenotic myocardial technetium-99m-teboroxime clearance kinetics after experimental ischemia and hyperemic stress.
The clearance kinetics of the perfusion tracer 99mTc-teboroxime were evaluated in post-stenotic and normal myocardium using dynamic planar gamma camera imaging in pre-instrumented dogs in the control state (n = 9) and following total occlusion (2 min), pharmacologic stress with adenosine [80 and 160 micrograms/kg/min] or dipyridamole, and rapid atrial pacing (220/min). Technetium-99m-teboroxime clearance in normal myocardium was accelerated by adenosine and by dipyridamole compared to the control state (8.9 +/- 1.1 and 9.3 +/- 1.9 min versus 11.9 +/- 1.8 min; p less than 0.05). Post-stenotic 99mTc-teboroxime clearance half-time was most significantly prolonged compared to nonoccluded contralateral perfusion zones by 160 micrograms/kg/min adenosine stress (11.2 +/- 3.7 versus 6.3 +/- 1.5 min) and by complete coronary occlusion (12.1 +/- 3.3 versus 6.6 +/- 1.2 min; both p less than 0.05). Differential tracer clearance from post-stenotic versus nonoccluded zones produced quantitative evidence of relative defect "redistribution" in 71% of maximal stress studies at a mean of 8.8 +/- 2.5 min postinjection. Sensitivity, specificity, and diagnostic accuracy of prolonged regional 99mTc-teboroxime clearance rates for post-stenotic perfusion abnormalities were 62%, 100% and 81% in maximal stress studies. Future clinical trials of exercise and nonexercise stress 99mTc-teboroxime imaging should consider these kinetic characteristics and examine the correlates of perfusion defect "redistribution."
Adenosine↗
Infection of an implantable cardioverter defibrillator: management without removal of the device in selected cases.
A case is presented in which an implantable cardioverter defibrillator (ICD) became infected in the abdominal wall pocket 5 weeks following implantation. There was no evidence clinically or by computed tomographic scan suggesting mediastinal extension of the infection. The infection was treated successfully by debriding the abdominal wall pocket followed by a combination of pocket irrigation with antibiotic solution, parenteral antibiotics, and long-term oral antibiotics. This conservative therapy was successful and avoided removal of the device.
Abdominal Muscles↗
Comparative effects of pacing-induced and flow-limited ischemia on left ventricular function.
We compared left ventricular (LV) myocardial blood flow and function accompanying severe demand ischemia (rapid atrial pacing in the presence of critical bilateral coronary stenoses) and supply ischemia (complete bilateral coronary occlusion) of the same ischemic regions in 14 pentobarbital-anesthetized dogs. Pacing-induced ischemia resulted in pronounced reductions in average regional epicardial blood flow (0.8 +/- 0.4 vs. control 1.2 +/- 0.4 [+/- SD] ml/g/min, p less than 0.05) and endocardial blood flow (0.4 +/- 0.1 vs. control 1.3 +/- 0.3 ml/g/min, p less than 0.05). More severe reductions in average regional epicardial and endocardial blood flow were seen after bilateral coronary occlusion (BCO) (0.3 +/- 0.3 and 0.1 +/- 0.1 vs. control 1.3 +/- 0.3 ml/g/min, p less than 0.05, respectively). Hemodynamics of postpacing ischemia (PPi) were consistently characterized by systolic impairment including depressed systolic contractile performance [(+)dP/dtmax 1,281 +/- 442 vs. control 2,173 +/- 775 mm Hg/sec, p less than 0.05], ventricular dilation (left ventricular [LV] end-diastolic dimension [EDD] 47.6 +/- 7.8 vs. control 44.7 +/- 8.6 mm, p less than 0.05), and an increase in LV end-diastolic pressure (EDP) (14.4 +/- 2.8 vs. control 4.2 +/- 2.8 mm Hg, p less than 0.05). Abnormalities in early and late diastolic function with PPi included increased time constant of isovolumic relaxation (78.0 +/- 40.4 vs. control 46.4 +/- 20.5 msec, p less than 0.05) and increased chamber stiffness (1.9 +/- 0.77 vs. control 0.81 +/- 0.55 mm Hg/mm, p less than 0.05), respectively. The LV diastolic pressure-dimension relation, however, shifted upward and to the right in eight of nine animals, whereas an upward shift was observed in only one animal. Thus, in this model of postpacing ischemia, we observed contractile failure and passive changes in diastolic function. Alterations in ventricular function occurred consistently earlier and to a greater extent during BCO than PPi, including higher LVEDP (25.3 +/- 8.1 vs. 14.9 +/- 6.6 mm Hg, p less than 0.05), greater ventricular dilation (delta LVEDD 4.9 +/- 2.5 vs. 3.5 +/- 2.8 mm, p less than 0.05), and reduced minor-axis dimension shortening (3.3 +/- 3.1% vs. 6.5 +/- 3.6%, p less than 0.05). To detect potential qualitative differences in ventricular function between the two types of ischemia, we evaluated hemodynamics at comparable loading conditions (30 seconds to 1 minute of BCO).(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
Antiphospholipid antibodies. A marker of lupus carditis?
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Antibodies↗
Acute hemodynamic changes during intravenous dipyridamole thallium imaging early after infarction.
In order to determine the safety and hemodynamic effects of intravenous dipyridamole infusion for thallium-201 scinitigraphy in patients with acute ischemic syndromes, 10 patients with recent uncomplicated myocardial infarction (7 +/- 2 days pre-test) had central pressures and cardiac output values measured serially in a coronary care unit during and after the administration of dipyridamole (0.56 mg/kg over 4 minutes) and following aminophylline reversal (50 to 150 mg intravenously) of dipyridamole effect. Cardiac medications were not discontinued. Double product did not change significantly (8522 +/- 1811 versus 9044 +/- 1701; p = NS). Serious ischemic events did not occur, although 20% of patients had noncardiac side effects and 30% developed greater than or equal to 1 mm ST segment depression with associated angina in one-third of these cases. The peripheral blood pressure and heart rate response did not predict the occurrence of myocardial ischemia. Dipyridamole significantly reduced systemic vascular resistance (1218 +/- 302 to 739 +/- 166 dyne/sec-1/cm-5; p less than 0.05) and increased cardiac index (3.1 +/- 0.7 to 4.7 +/- 1.0 L/min/m2; p less than 0.05) within approximately 10 minutes, in association with a significant increase in pulmonary capillary wedge pressure (13 +/- 5 to 17 +/- 6 mm Hg; p less than 0.05). Three patients developed silent new "V" waves in their pulmonary capillary wedge pressure tracing, associated with anterior thallium redistribution. All three patients with newly elevated wedge pressures (greater than 15 mm Hg) had both thallium-201 redistribution and multivessel coronary disease.(ABSTRACT TRUNCATED AT 250 WORDS)
Aminophylline↗
Diltiazem attenuates the inotropic and peripheral vascular effects of cardiac glycosides.
The influence of diltiazem on the hemodynamic effects of ouabain in 10 preinstrumented awake dogs was studied. Mean aortic pressure increased from 102 to 119 mm Hg with ouabain (p less than 0.05), an effect that was attenuated by pretreatment with diltiazem. The increase in systemic vascular resistance of 30% with ouabain was ablated by prior diltiazem. Heart rate did not significantly change with ouabain or with diltiazem plus ouabain, but intravenous diltiazem alone produced a reflex increase in heart rate of 26%. Left ventricular (LV) end-diastolic dimension was significantly greater with ouabain alone, but not with ouabain after pretreatment with diltiazem. LV dP/dt max increased by 40% with ouabain alone, but by only 23% (p less than 0.001) after pretreatment with diltiazem plus ouabain. When observed at matched preload and heart rate, diltiazem markedly attenuates the positive inotropic and peripheral arterial constrictive effects of acute ouabain administration in the conscious animal with normal LV function.
Animals↗
Effect of digoxin and vasodilators on left ventricular function in aortic regurgitation.
In order to assess the relative value of digoxin, nifedipine and hydralazine on left ventricular performance at rest and during exercise, we studied 10 men with moderately severe chronic aortic regurgitation using two-dimensional echocardiography. Digoxin after one month at therapeutic serum levels increased resting ejection fraction as compared to control [0.54 +/- 0.08 (SD) vs 0.47 +/- 0.08, respectively, P less than 0.03]. Ejection fraction decreased during exercise but the difference between digoxin and control was maintained. Stroke volume also was higher on digoxin than control at rest (93 +/- 15 vs 83 +/- 17 ml, P less than 0.02) and the larger stroke volume on digoxin was maintained during exercise. By contrast, stroke volume was reduced by one month of therapy with maximally tolerated nifedipine doses compared to control (74 +/- 8 vs 83 +/- 17 ml, P = 0.03) and this difference was maintained during exercise. Hydralazine in doses up to 225 mg/day for one month produced no significant changes in left ventricular performance compared to control at rest or during exercise. However, compared to digoxin ejection fraction at peak exercise was significantly less on hydralazine (0.39 +/- 0.9 vs 0.52 +/- 10, P less than 0.02). These data suggest that digoxin improved left ventricular performance and may be of benefit in the treatment of patients with chronic aortic regurgitation.
Adult↗
Response of blood pressure, cardiac output, peripheral resistance, and exercise performance to substitution of calcium blocker for beta-blocker plus thiazide diuretic therapy in patients with both systemic hypertension and mild stable angina.
We studied 14 patients to determine whether sustained-release diltiazem is a satisfactory long-term substitute for the combination of propranolol plus hydrochlorothiazide (HCTZ), control phase, in the treatment of systemic hypertension with coexisting chronic stable angina pectoris. All patients had either one- or two-vessel coronary disease and normal left ventricular systolic function. Measurements were made during the control phase and 4 and 8 weeks after substitution of sustained-release diltiazem. Only the sitting blood pressure was available before the control phase (pretreatment). Blood pressure and heart rate were measured with patients supine, sitting, and 5 minutes after standing. Cardiac output was measured in the supine position using a computerized Doppler system, and stroke volume, mean arterial pressure, and total systemic resistance were calculated. Symptom-limited modified Bruce protocol treadmill tests were performed to determine time to onset of 1 mm ST segment depression, time to termination of exercise, reason for cessation of exercise, and maximum rate-pressure product. The patients were initially receiving 160-240 mg/day of propranolol (40-60 mg q.i.d.) plus 25-50 mg/day of HCTZ and, subsequently, 12 of 14 had substitution with 240 mg/day (120 mg b.i.d.) of sustained-release diltiazem, and two received 360 mg/day with one of these patients also receiving 50 mg/day of HCTZ. These patients are a subset of a larger group of patients in whom the response of blood pressure alone has been previously reported. Diltiazem resulted in reduction of blood pressure equivalent to that with the propranolol plus HCTZ combination.(ABSTRACT TRUNCATED AT 250 WORDS)
Adrenergic beta-Antagonists↗
Nadolol versus diltiazem and combination for preventing exercise-induced ischemia in severe angina pectoris.
Combination beta-blocker and calcium antagonist therapy has been shown to be superior to monotherapy with either class of drugs in the treatment of patients with severe angina pectoris. Some combinations of these agents have resulted in an increased frequency of adverse effects. Although nadolol and diltiazem have low incidences of side effects as monotherapy, little is known about their combination. Thus, 18 patients with angina pectoris despite medical therapy were randomly assigned to 3-week periods of nadolol (160 mg/day), diltiazem (240 mg/day) or their combination. At the end of each treatment period, treadmill exercise testing and rest and peak bicycle exercise 2-dimensional echocardiography were performed. The heart rate-systolic blood pressure product was decreased most at peak treadmill exercise with the combination therapy versus monotherapy with either nadolol or diltiazem (12 vs 14 vs 22 x 10(3), respectively, p less than 0.05). Exercise duration did not differ with any of the 3 regimens, but the number of patients without angina during exercise was lowest with the combination therapy versus nadolol or diltiazem alone (5, 10 and 11, respectively, p less than 0.05); similar results were noted with the number of patients developing 1-mm ST depression on the exercise electrocardiogram (6, 10 and 13, respectively, p less than 0.05). The left ventricular ejection fraction at rest and during peak exercise was similar among the 3 treatments. The therapeutic combination of nadolol and diltiazem is well tolerated and results in less evidence of myocardial ischemia during exercise than monotherapy with either agent.
Aged↗
The care of elderly patients with cardiovascular disease.
Cardiovascular disease is a major clinical problem in the elderly, with coronary heart disease the most frequent cause of death and with hypertension present in as many as 50% of these patients. The cardiovascular manifestations of aging must be differentiated from those due to disease. There are clinical manifestations and responses to therapy in the elderly that differ from those in younger patients. The extent of diagnostic and therapeutic procedures undertaken should be based on the patient's physiologic age, the presence and severity of concomitant diseases, mental status and cognitive ability, and the patient's expectations from medical care. Preventive approaches are also warranted.
Age Factors↗
Bedside diagnosis of systolic murmurs.
The diagnostic accuracy of bedside maneuvers in the evaluation of patients with systolic murmurs has not been assessed objectively. Therefore, we evaluated 50 patients with documented systolic murmurs and compared all standard bedside techniques. Murmurs originating within the right-sided chambers of the heart were best differentiated from all other murmurs by augmentation of their intensity with inspiration (100 percent sensitivity, 88 percent specificity) and diminution of their intensity with expiration (100 percent sensitivity, 88 percent specificity). The murmur of hypertrophic cardiomyopathy was distinguished from all other murmurs by an increase in intensity with the Valsalva maneuver (65 percent sensitivity, 96 percent specificity) and during squatting-to-standing action (95 percent sensitivity, 84 percent specificity), and by a decrease in intensity during standing-to-squatting action (95 percent sensitivity, 85 percent specificity), passive leg elevation (85 percent sensitivity, 91 percent specificity), and handgrip (85 percent sensitivity, 75 percent specificity). The murmurs of mitral regurgitation and ventricular septal defect had parallel responses to all maneuvers, but could be differentiated from other systolic murmurs by augmentation of their intensity with handgrip (68 percent sensitivity, 92 percent specificity) and during transient arterial occlusion (78 percent sensitivity, 100 percent specificity), and by a decrease in their intensity during the inhalation of amyl nitrite (80 percent sensitivity, 90 percent specificity). No single maneuver identified the murmur of aortic stenosis, but the diagnosis could be made by exclusion. Although no single maneuver is 100 percent accurate in diagnosing the cause of a systolic murmur, its origin can be determined accurately at the bedside by observation of the response to a combination of maneuvers.
Adolescent↗
Left atrial enlargement: an early sign of hypertensive heart disease.
Left atrial abnormality on the electrocardiogram (ECG) has been considered an early sign of hypertensive heart disease. In order to determine if echocardiographic left atrial enlargement is an early sign of hypertensive heart disease, we evaluated 10 normal and 14 hypertensive patients undergoing routine diagnostic cardiac catheterization for echocardiographic left atrial enlargement. All patients had normal coronary arteriography, sinus rhythm, normal left ventricular volumes and function, no valvular disease, and no echocardiographic or ECG left ventricular hypertrophy. No patient met ECG criteria for left atrial abnormality. The mean left atrial dimension was 3.46 +/- 0.3 cm in normal individuals versus 4.04 +/- 0.3 cm in the hypertensive patients (p less than 0.01). The left atrial index was also higher in the hypertensive group, 2.18 +/- 0.45 versus 1.88 +/- 0.10 cm/m2 (p less than 0.05), and the left atrial-to-aortic root dimension ratio was significantly higher in the hypertensive group, 1.36 +/- 0.20 versus 1.17 +/- 0.07 (p less than 0.01). We conclude that echocardiographic left atrial enlargement may be an early sign of hypertensive heart disease in patients with no other discernible cause of left atrial enlargement.
Cardiomegaly↗