Coronary blood flow reserve in acute aortic regurgitation.

OBJECTIVES: This study sought to determine the impact of acute aortic regurgitation on coronary blood flow reserve and phasic epicardial coronary blood flow in closed-chest dogs. BACKGROUND: Hemodynamic changes in acute aortic regurgitation are known to precipitate myocardial ischemia. Coronary blood flow reserve has not been studied in closed-chest experimental preparations with acute aortic regurgitation. METHODS: Graded temporary acute aortic regurgitation was produced in 11 mongrel dogs. Phasic coronary blood flow velocities were measured using a Doppler guide wire. Coronary flow reserve was defined as the ratio of the time average of spectral peak velocity after administration of papaverine to that of the baseline state. RESULTS: Under control conditions (mean [+/- SEM] diastolic blood pressure 82.2 +/- 4.5 mm Hg), coronary flow reserve was 3.51 +/- 0.27 with predominantly diastolic epicardial coronary blood flow. With mild acute aortic regurgitation (diastolic blood pressure 61.8 +/- 3.0 mm Hg), coronary flow reserve decreased to 2.38 +/- 0.27, with an increase in phasic systolic epicardial coronary blood flow. At the onset of moderate acute aortic regurgitation (diastolic blood pressure 42.1 +/- 0.9 mm Hg), coronary flow reserve declined further to 1.46 +/- 0.12, and the phasic systolic epicardial coronary blood flow became more prominent. With severe aortic regurgitation (diastolic blood pressure 29.2 +/- 2.2 mm Hg), coronary flow reserve reached 1.20 +/- 0.05, and the phasic epicardial coronary blood flow pattern was found to be predominantly systolic with retrograde diastolic flow. The ratio of diastolic to systolic pressure-time indexes with severe aortic regurgitation suggested subendocardial underperfusion. CONCLUSIONS: This study demonstrates a marked decline in coronary blood flow reserve and documents a progressive change in the phasic epicardial blood flow to a predominantly systolic pattern with increasing degrees of acute aortic regurgitation.

Vasodilator therapy in chronic asymptomatic aortic regurgitation: enalapril versus hydralazine therapy.

OBJECTIVES: This study attempted to evaluate the long-term efficacy of enalapril versus hydralazine therapy on left ventricular volume, mass and function as well as on the renin-angiotensin system in chronic asymptomatic aortic regurgitation. BACKGROUND: We tested the hypothesis that early administration of a vasodilator drug might be able to reduce left ventricular dilation and mass expansion. Because the renin-angiotensin system may be activated in chronic aortic regurgitation, early enalapril therapy might be beneficial. METHODS: Between 1990 and 1993, 76 asymptomatic nonrheumatic patients with mild to severe chronic aortic regurgitation were enrolled in a randomized, double-blind trial comparing enalapril with hydralazine. All patients underwent serial noninvasive studies. Seventy patients completed the 12-month follow-up. RESULTS: At 1 year, patients receiving enalapril had a significant reduction in left ventricular end-diastolic and end-systolic volume indexes (124 +/- 15 vs. 108 +/- 17 ml/m2, p < 0.01; 50 +/- 12 vs. 40 +/- 14 ml/m2, p < 0.01, respectively) and mass index (131 +/- 16 vs. 113 +/- 19 g/m2, p < 0.01), whereas hydralazine therapy showed no significant changes. Both regimens not only had a significant reduction in left ventricular mean wall stress but also had a mild increase in exercise duration. Only enalapril therapy achieved a significant inhibition of the renin-angiotensin system, in contrast to hydralazine therapy. Moreover, the multiple r2 value from the analysis for end-diastolic volume index using the two variables of age and treatment drugs was 72.1% (p < 0.01). CONCLUSIONS: Both regimens decrease left ventricular mean wall stress. Enalapril therapy achieves significant left ventricular mass regression, left ventricular end-diastolic and end-systolic volume index reduction and renin-angiotensin system suppression. These findings suggest that early unloading enalapril therapy has the potential to favorably influence the natural history of chronic aortic regurgitation.

Ethics in cardiovascular medicine. Task Force II: The relation of cardiovascular specialists to patients, other physicians and physician-owned organizations.

1. The American College of Cardiology acknowledges the continuum of changing societal, medical and economic perspectives affecting traditional medical ethics. Primacy of patient responsibility remains paramount to the cardiovascular specialist who at the same time should participate in the development of broader societal programs. 2. Medical decisions should be freely and jointly formulated by the patient and the cardiovascular specialist with appropriate sensitivity to such matters as mental competence, pertinent medical information and standards of care, sufficient time for contemplation, informed consent, patient right of refusal, physician right to refuse to provide inappropriate care and the right of patient, physician or third party payer to seek consultation or additional opinions. 3. The cardiovascular specialist should make a special effort to clarify and document patient preferences regarding end-of-life treatment through some form of advance directive. 4. The cardiovascular specialist bears a moral obligation to provide medical care to any patient who is HIV positive or has AIDS. 5. A conflict of interest occurs when a cardiovascular specialist places personal or financial interest ahead of the welfare and health of a patient. Professional accountability should be established through local or regional peer review. 6. The American College of Cardiology encourages and supports a renewed dedication to the principles of medical ethics, particularly in the field of cardiovascular disease. Cardiovascular specialists are encouraged to participate in the promulgation of medical ethics by teaching and by example, individually and with others.

Quantification of left to right atrial shunts with velocity-encoded cine nuclear magnetic resonance imaging.

OBJECTIVES: The purpose of this study was to evaluate the ability of velocity-encoded nuclear magnetic resonance (NMR) imaging to quantify left to right intracardiac shunts in patients with an atrial septal defect. BACKGROUND: Quantification of intracardiac shunts is clinically important in planning therapy. METHODS: Velocity-encoded NMR imaging was used to quantify stroke flow in the aorta and in the main pulmonary artery in a group of patients who were known to have an increased pulmonary to systemic flow ratio (Qp/Qs). The velocity-encoded NMR flow data were used to calculate Qp/Qs, and these values were compared with measurements of Qp/Qs obtained with oximetric data derived from cardiac catheterization and from stroke volume measurements of the two ventricles by using volumetric data from biphasic spin echo and cine NMR images obtained at end-diastole and end-systole. RESULTS: Two independent observers measured Qp/Qs by using velocity-encoded NMR imaging in 11 patients and found Qp/Qs ranging from 1.4:1 to 3.9:1. These measurements correlated well with both oximetric data (r = 0.91, SEE = 0.35) and ventricular volumetric data (r = 0.94, SEE = 0.30). Interobserver reproducibility for Qp/Qs by velocity-encoded NMR imaging was good (r = 0.97, SEE = 0.20). CONCLUSIONS: Velocity-encoded NMR imaging is an accurate and reproducible method for measuring Qp/Qs in left to right shunts. Because it is completely noninvasive, it can be used to monitor shunt volume over time.

Ejection fraction response to supine exercise in asymptomatic aortic regurgitation: relation to simultaneous hemodynamic measurements.

The change in ejection fraction during exercise is frequently employed as a measure of left ventricular functional reserve in patients with aortic regurgitation. However, little information is available about its relation to invasive measurements of cardiac performance. Therefore, simultaneous hemodynamic measurements and supine exercise blood pool scintigraphy were performed in 14 patients with severe, asymptomatic or minimally symptomatic aortic regurgitation associated with cardiomegaly but preserved left ventricular function at rest. Their hemodynamic measurements at rest were normal and their exercise capacity was excellent. When the patients were categorized into those patients whose ejection fraction increased or did not decrease by more than 0.05 (Group 1) and those whose ejection fraction decreased by more than 0.05 (Group 2), important differences were apparent. Echocardiographic, radionuclide and hemodynamic measurements at rest in the two patient groups were similar, but Group 1 exhibited a greater increase in cardiac index during supine exercise (2.8 +/- 0.4 to 10.0 +/- 1.8 versus 2.7 +/- 0.5 to 6.9 +/- 1.0 liters/min per m2; p less than 0.005) and a lesser increase in pulmonary capillary wedge pressure (13 +/- 4 to 19 +/- 7 versus 12 +/- 4 to 31 +/- 8 mm Hg; p less than 0.01). The severity of regurgitation decreased during exercise in all patients, but end-diastolic volume decreased and end-systolic volume decreased or was unchanged in Group 1, whereas end-diastolic volume was unchanged and end-systolic volume increased in Group 2.(ABSTRACT TRUNCATED AT 250 WORDS)

Etiology of the Austin Flint murmur.

OBJECTIVES: The aim of the study was to determine the mechanism of the Austin Flint murmur. BACKGROUND: More than 100 years after the initial description of the Austin Flint murmur, the etiology of the murmur remains unclear. METHODS: M-mode and two-dimensional echocardiography, conventional and color flow Doppler study, and cine nuclear magnetic resonance (cine NMR) imaging were performed in 24 patients with clinically moderate or severe aortic regurgitation. Mitral valve area was determined by planimetry and pressure half-time measurement. Overlap of the aortic regurgitation and mitral inflow jets was graded 0 (no overlap) to 4 (marked overlap) by Doppler study and cine NMR imaging. The volume of signal loss resulting from turbulent blood flow secondary to the aortic regurgitation jet was determined on cine NMR images, and the extent of contact with the left ventricular endocardium was graded 0 (no contact) to 4 (extensive contact). RESULTS: The presence of an Austin Flint murmur did not correlate with mitral valve area (2.7 +/- 0.8 cm2 with the murmur vs. 2.5 +/- 0.7 cm2 without), overlap of the aortic regurgitation and mitral flow jets (3 +/- 1 vs. 2.3 +/- 1.2), diastolic mitral regurgitation (50% vs. 71%) or fluttering of the anterior mitral valve leaflet (70% vs. 50%). The presence of an Austin Flint murmur correlated best with the volume of signal loss associated with the aortic regurgitation jet on cine NMR imaging (65 +/- 16 ml with the murmur. vs. 38 +/- 11 ml without, p less than 0.001) and the extent of contact of this signal loss with the left ventricular endocardium (2.9 +/- 0.5 vs. 1.5 +/- 0.4, p less than 0.0001). CONCLUSIONS: The Austin Flint murmur is caused by the aortic regurgitation jet abutting the left ventricular endocardium, resulting in the generation of a low-pitched diastolic rumbling.

Dissecting aortic aneurysm manifesting as acute pericarditis.

Two patients with coarctation of the aorta initially had acute idiopathic pericarditis with anterior pleuritic chest pain as the chief complaint. A pericardial friction rub was present in both patients. Both patients died suddenly. At autopsy, they were found to have a dissecting aneurysm of the ascending aorta with extension into the pericardial space; acute pericardial tamponade was the cause of death. We recommend that when a patient with coarctation of the aorta is admitted with pericarditis, aortic dissection should be considered and appropriate diagnostic procedures undertaken. In all young patients with acute pericarditis there should be careful palpation of the femoral pulses and review of the chest x-ray film for rib notching.

Echocardiographic appearance of ruptured aortic cusp.

Serial echocardiograms of a patient with enterococcal endocarditis and aortic insufficiency suggested the presence of vegetations on the aortic valve with progression of the lesion to frank prolapse of an aortic valve cusp. At surgery, the patient was found to have a flail noncoronary cusp to which an 8 mm vegetation was adherent. Anatomic correlations are presented, and a possible mechanism for the unusual echographic findings is discussed.

Congenital bicuspid aortic valve after age 20.

The bicuspid aortic valve is recognized as a frequent cause of aortic stenosis in adults. Aortic stenosis has been reported to occur in as many as 72 percent of adults with a congenital bicuspid aortic valve, with peak incidence occurring in the 5th and 6th decades of life. Review of the clinical records of 152 patients aged 20 years and older found to have a bicuspid aortic valve at autopsy revealed aortic stenosis in only 28 percent. The incidence of aortic stenosis increased progressively with age; 46 percent of patients over age 50 years and 73 percent over age 70 years had some degree of stenosis. The stenotic valves were obstructed by nodular, calcareous masses but commissural fusion was present in only eight cases. The largest group of patients in the series (40 percent) died of infective endocarditis; 77 percent of these were under age 50 years. Primary aortic regurgitation without infective endocarditis was uncommon. Thirty-two percent of the patients in this series had an apparently normally functioning aortic valve, and this rate remained relatively constant with increasing age; 37 percent of patients over age 50 years and 27 percent over age 70 years had an apparently normal valve. The bicuspid aortic valve in patients over age 20 does not invariably become stenotic or insufficient.

Congenital aortic stenosis secondary to dysplasia of congenital bicuspid aortic valves without commissural fusion.

The hearts of nine children with clinical evidence of congenital valve stenosis and a congenital bicuspid aortic valve were reviewed. Aortic stenosis was diagnosed on the basis of cardiac catheterization data in four patients, operative findings in two and auscultatory findings in three. The patients were 1 month to 9 years old; six were male and three female. In each patient the two commissures of the valve were free to the aortic wall. The cusps were thickened, rolled and redundant; microscopic studies revealed that they consisted of immature loose connective tissue consistent with a dysplastic or incompletely differentiated valve. The valve orifice was obstructed by the dysplastic cusps, and dysplastic changes rather than the commissural fusion were responsible for the observed aortic stenosis. These valves do not appear amenable to valvotomy because obstruction is due to the abnormal valve tissue. These findings may explain the occasional poor results of valvotomy in infants and children with congenital aortic valve stenosis.

Regional left ventricular wall thickening by magnetic resonance imaging: evaluation in normal persons and patients with global and regional dysfunction.

Gated magnetic resonance imaging (MRI) provides excellent anatomic evaluation of the heart, but its capability for assessing cardiac physiology is less clear. Accordingly, regional left ventricular (LV) wall thickening was evaluated by multiphasic transverse images in 37 patients with a variety of myocardial diseases and in 9 normal subjects. Angiography and 2-dimensional echocardiography (2-D echo) were used for comparison. End-diastolic and end-systolic wall thickness, absolute systolic wall thickening and percent systolic wall thickening were determined in 7 regions. Mean systolic wall thickening in normal subjects was not significantly different among the regions. However, there was considerable individual variation in wall thickening, ranging from 18 to 100%. Patients with LV hypertrophy (n = 4), amyloid cardiomyopathy (n = 1), constrictive pericarditis (n = 5), and hypertrophic cardiomyopathy (n = 3) had absolute and percent systolic wall thickening within normal limits. Infarcted segments in patients with ischemic heart disease (n = 17) had reduced absolute and percent systolic wall thickening, often combined with diastolic wall thinning, whereas mean percent systolic wall thickening in adjacent normal myocardial regions was higher than in normal volunteers (p less than 0.001). In patients with coronary artery disease, MRI had a sensitivity and specificity of 93% in detecting regional wall motion abnormalities. Because sagittal images were not acquired, inferior wall motion abnormalities were not assessed by MRI due to parallel wall sectioning in transverse images.(ABSTRACT TRUNCATED AT 250 WORDS)

Risk of ventricular arrhythmias in hypertensive men with left ventricular hypertrophy.

The echocardiographic predictors of ventricular arrhythmias are reported for the Hypertension Arrhythmia Reduction Trial. Men with mild hypertension were withdrawn from their diuretic therapy and repleted with 40 mEq/day of oral potassium and 20 mEq/day of oral magnesium for 1 month. M-mode echocardiography and 24-hour continuous ambulatory electrocardiography were performed on 123 men, mean age 62 years. Forty-eight men (39%) had echocardiographic evidence of left ventricular (LV) hypertrophy defined as an LV mass index greater than 134 g/m2 and this finding was not related to the presence of LV hypertrophy on electrocardiogram or to age. Men who had echocardiographic LV hypertrophy were more likely than men without echocardiographic LV hypertrophy to have greater than or equal to 30 ventricular premature complexes (VPCs)/hr (odds ratio = 2.7; 95% confidence interval = 0.9, 8.0), multiform extrasystoles (odds ratio = 1.7; confidence interval = 0.8, 3.7), episodes of ventricular tachycardia (odds ratio = 2.3; confidence interval = 0.7, 7.1) and the combination of frequent (greater than or equal to 30 VPCs/hr) or complex (ventricular couplets, multiform extrasystoles or episodes of ventricular tachycardia) ventricular arrhythmia (odds ratio = 1.7; confidence interval = 0.8, 3.5). Similar associations between echocardiographic LV hypertrophy and ventricular arrhythmias were observed on 24-hour tracings obtained on entry to the study (before electrolyte repletion) in the 96 men who were taking diuretics at this time. The combination of a frequent or complex arrhythmia was also more common in men aged 60 to 70 compared to men aged 35 to 59 (odds ratio = 3.4; confidence interval = 1.4, 8.2).(ABSTRACT TRUNCATED AT 250 WORDS)

Silent myocardial ischemia in men with systemic hypertension and without clinical evidence of coronary artery disease.

The prevalence, characteristics and circadian pattern of silent myocardial ischemia, and its association with ventricular arrhythmias was studied in hypertensive men aged 35 to 70 years (mean 61) without clinical cardiac disease. Participants were withdrawn from diuretic treatment and received 1 month of oral electrolyte repletion with 40 mmol of potassium chloride, and 400 mg of magnesium oxide daily. Twenty-four-hour Holter monitoring was then performed. Episodes of silent myocardial ischemia occurred in 50 of 186 men (27%) and lasted from 2 to 289 minutes (mean 30 and median 18). Statistical analysis comparing the interval from midnight to 6 A.M. with each of the other three 6-hour time intervals revealed that participants were less likely to have silent myocardial ischemia in this period (p less than 0.01 for each comparison) than at other times of the day. There was little difference in the proportion of men with a frequent or complex ventricular arrhythmia during the entire day or within 1 hour of the silent myocardial ischemic episode (or during a comparable time period) comparing those with to those without silent myocardial ischemia. These findings indicate that silent myocardial ischemia occurs in approximately 25% of an older population of hypertensive men without history of symptomatic cardiac disease. The circadian pattern of frequency of silent ischemic events in men free of clinical cardiac disease is similar to that reported for patients with cardiac disease and coincides with that reported for sudden death. There was no significant association between silent myocardial ischemia and ventricular arrhythmias.

Tricuspid insufficiency due to nonpenetrating trauma.

This case of tricuspid insufficiency due to nonpenetrating trauma involved a male patient who had received major chest trauma in an automobile accident, had a nonholosystolic murmur that increased slightly during inspiration on standing, and tranient electrocardiographic findings of right bundle branch block. Unlike findings in previous cases, the right atrial V wave was not dominant and was less than 8 mm Hg. An echocardiogram indicating right ventricular volume overload was an essential diagnostic tool that led to cardiac catheterization and definitive diagnosis.

Spontaneous graft closure in anomalous origin of the left coronary artery.

Several reports of successful correction of anomalous origin of the left coronary artery from the pulmonary artery utilizing a graft to the ascending aorta have demonstrated the feasibility of this procedure. The patient described in this report developed proved delayed occlusion of the saphenous vein graft with a fatal outcome. This was a result of intimal fibrous hyperplasia identical to that seen in adults following the placement of the saphenous vein bypass graft for treatment of atherosclerotic coronary disease.

Coronary atherosclerosis in mitral stenosis.

Eighty-two patients with mitral stenosis underwent cardiac catheterization with coronary angiography. Twenty-one patients (26 percent) had coronary artery disease. Characteristics of the mitral valve area, cardiac output, pulmonary artery pressure, pulmonary vascular resistance, left ventricular end-diastolic pressure, left ventricular ejection fraction, and atypical chest pain did not correlate with findings of angina pectoris or of coronary artery disease; however, there was correlation with sex, age, and angina. Coronary artery disease occurred only after the age of 40 years and was more frequent in males with angina. Coronary artery disease could not be ruled out in patients with mitral stenosis, especially those over age 40, without coronary arteriography.

Quadricuspid semilunar valves.

Forty-seven cases of quadricuspid semilunar valves which were autopsied were reviewed. The ratio of quadricuspid pulmonic valve to quadricuspid aortic valve was 5:1. Among the 35 patients with quadricuspid pulmonic valves, there were ten patients with clinical and pathologic evidence of coexisting congenital cardiac defects, eight of which resulted in severe cyanotic heart disease in infancy. In the remaining 25 patients the quadricuspid pulmonic valve was an incidental finding at autopsy. Three of the seven patients with quadricuspid aortic valves had aortic insufficiency, while the remaining four had no other clinical or pathologic evidence of congenital heart disease.

Giant coronary pseudoaneurysm. Five-year follow-up after bypass grafting.

A roentgenogram of the shoulder in a 25-year-old man with an athletic injury revealed a large mass along the left heart border. Evaluation with coronary arteriography established the diagnosis of a massive aneurysm of the left anterior descending coronary artery. The aneurysm was excised and a saphenous vein bypass graft was placed into the distal artery. Histologic examination revealed that the excised segment was a false aneurysm. Five years postoperatively, the patient is asymptomatic and the graft remains widely patent.

Reappraisal of continuous positive airway pressure therapy in acute cardiogenic pulmonary edema. Short-term results and long-term follow-up.

To investigate whether serial incremental continuous positive airway pressure (CPAP) has any short-term or long-term advantages over face-mask oxygen therapy by way of intrapulmonary shunt reduction, 100 patients admitted to the coronary care unit for the treatment of acute cardiogenic pulmonary edema were studied. All patients received Swan-Ganz catheterization. Hemodynamic and pulmonary function parameters were recorded over the next 6 h, and the patients were followed until hospital discharge. All survivors received regular follow-up at 1-month intervals in the outpatient clinic. During the first-stage investigation period (3 h) PaO2 in the CPAP group showed a significant increase, whereas the intrapulmonary shunt and alveolar-arterial oxygen tension gradient (P[A-a]O2) was significantly reduced (p < 0.005). The CPAP group had significantly lower rate-pressure product and higher stroke volume index compared with the control group. The therapeutic failure rate over 6 h was 24% in the CPAP group and 50% in the control group (p < 0.01). The CPAP group had a significantly lower incidence of tracheal intubation and ventilator therapy than the control group; however, there was no significant difference in short-term mortality and hospital stay between the two groups. In conclusion, although study size was not large enough to demonstrate a difference in mortality, CPAP therapy resulted in physiologic cardiovascular and pulmonary function improvement and significantly reduced the need for intubation; however, it did not decrease mortality in patients with acute cardiogenic pulmonary edema, and a much larger study is needed to investigate this possibility.

Echocardiography in serial evaluation of left ventricular systolic and diastolic function: importance of image acquisition, quantitation, and physiologic variability in clinical and investigational applications.

Quantitative echocardiography is frequently used for serial evaluation of left ventricular performance. This prospective study was designed to determine the extent to which the acts of image acquisition and quantitation, and the subjects themselves, affect total variability in two-dimensional and Doppler echocardiographic indexes of left ventricular morphology and performance. Therefore, two technicians and two readers acquired and analyzed 60 echocardiograms from 15 normal subjects, each of whom was studied four times (twice on each of two visits). Analysis of variance based on generalizability theory was used to estimate the magnitude of these variability sources by calculating standard deviations (SD) and used to estimate their contribution to total variability. Of the two-dimensional echocardiographic indexes tested, ejection fraction varied least (SD, 6.6%) and left ventricular mass varied most (SD, 35.3 gm). Of the Doppler indexes, normalized early diastolic filling velocity integral varied least (SD, 8.4%) and deceleration time varied most (SD, 48.6 msec). Technical (image acquisition and quantitation) variability contributed most (and subject variability least) to total variability of stroke volume (68%) and deceleration time (67%). Technical variability contributed least (and subject variability most) to variability of ejection fraction (43%) and diastolic filling time (25%). The acts of image acquisition and quantitation varied more between than within technicians and readers. Peak atrial filling velocity and the ratio of peak early to atrial filling velocity significantly differed between technicians. Left ventricular ejection fraction, left ventricular mass, peak atrial filling velocity, early filling integral, and deceleration of early filling differed significantly between readers. Therefore the acts of image acquisition and quantitation, and subject variability itself, all contribute to total variability in echocardiographic indexes. Changes seen on clinical studies should be interpreted as abnormal only when exceeding the total variability originating from these sources. Generalizability theory allows one to tailor strategies to reduce variability. These strategies include increasing the number of observations, readers, and technicians for any given "baseline" study and using the same readers and technicians for sequential follow-up studies.