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Long-term left ventricular assist device use before transplantation.

Between September 1992 and April 1995, 19 patients at the authors' institution received pneumatic, pulsatile left ventricular assist devices (LVADs) for bridging to cardiac transplantation. The mean (+/- SD) age of the patients was 51 +/- 14 years (range, 19-64 years). Nine (47%) patients had end-stage idiopathic cardiomyopathy, five (26%) had ischemic cardiomyopathy, and five (26%) other recipients were in cardiogenic shock caused by acute myocardial infarction (AMI). Fifteen (79%) patients were supported with an intraaortic balloon pump or centrifugal LVAD at the time of LVAD insertion (duration, 5.5 +/- 4.1 days). Aprotinin was given to limit bleeding; heparin, followed by warfarin sodium, was used for anticoagulation. A vigorous exercise and nutrition protocol was followed. Cardiac index averaged 2.94 +/- 0.87 L/min/m2 immediately after the implantation procedure. No patient required placement of a right VAD. Average duration of LVAD support was 45 +/- 39 days (range, 3-153 days). Major complications included bleeding requiring reoperation (three patients); cerebrovascular accident (three patients); and severe dysrhythmias requiring direct current cardioversion (four patients). Fourteen (74%) patients underwent transplantation, with one patient still being mechanically supported. All of the patients receiving transplants were discharged from the hospital. Of the individuals who died while supported with the LVAD, 75% were patients with AMI. Timely application of LVADs as part of the interdisciplinary management of end-stage heart disease has generated excellent results for transplant candidates. Right ventricular dysfunction has not necessitated right VAD placement in the authors' experience. Patients with AMI have a higher risk of death while being supported with the device than do more chronically ill recipients.

Adult↗

Effects of on-pump versus off-pump coronary artery bypass graft surgery on right ventricular function.

OBJECTIVES: Right ventricular dysfunction is a possible cause of cardiac failure after coronary surgery. The use of cardiopulmonary bypass is regarded as a major cause for its occurrence, and it has been postulated that performing coronary surgery without cardiopulmonary bypass might reduce ventricular dysfunction. Therefore, this prospective, randomized, controlled study tested the hypothesis that off-pump coronary surgery would better preserve right ventricular systolic and diastolic function than conventional bypass surgery. METHODS: Fifty patients scheduled for elective coronary artery bypass surgery were randomly assigned to conventional or off-pump surgery. Right ventricular function was assessed by intraoperative transesophageal echocardiography immediately before and after coronary surgery. Right ventricular ejection fraction was used as a marker of global systolic function and tricuspid early/late (atrial) ratio as a marker of the global diastolic function. Peak systolic and early diastolic velocities of the lateral tricuspid annulus were studied to assess systolic and diastolic function in the area of the right ventricular free wall. RESULTS: Surgery was completed according to randomization in 48 of 50 patients. Preoperative characteristics were similar in both groups. Intraoperative differences between the two groups included a higher volume of allogeneic blood transfusion in the conventional surgery group. At the end of surgery, global systolic right ventricular function was similarly maintained and diastolic function similarly impaired in both groups. There were no significant intergroup differences in any of the echocardiographic markers of right ventricular function. CONCLUSIONS: Off-pump surgery did not better preserve right ventricular systolic and diastolic function than did conventional coronary surgery.

Aged↗

[Right ventricular insufficiency in patients in the early periods after orthotopic transplantation of donor heart].

The function of transplanted heart in the early postoperative period is analyzed in 20 patients operated on at the Research Center of Surgery of the Russian Academy of Medical Sciences. Cardiac function was assessed by a complex of hemodynamic parameters, among which were the ratio between the ventricular stroke index and end diastolic pressure in the ventricle. Right-ventricular dysfunction of varying severity was detected in all the patients in the immediate postoperative period. Three variants of right-ventricular insufficiency were singled out: isolated right-ventricular insufficiency with increased (20%) and normal (45%) total vascular resistance and right-ventricular insufficiency combined with left-ventricular insufficiency (35%). Isolated right-ventricular insufficiency could be, as a rule, treated by combined intensive care including sympathomimetics and vasodilators. A combination of right-ventricular and left-ventricular insufficiency, which may be caused by incompatability between the sizes of the donor and recipient, as well as hypoxic and metabolic cardiac injury in donor body, is prognostically infavorable, for it requires intensive inotropic therapy and is associated with a high mortality.

Adult↗

Elevations of CK-MB following pulmonary embolism. A manifestation of occult right ventricular infarction.

To determine the frequency and etiology of elevations of CK-MB in patients with pulmonary emboli, we studied 52 patients with well-documented emboli and the absence of known ischemic heart disease or ECG changes suggestive of acute infarction. All patients were evaluated with serial CK-MB determinations at 8-h intervals. All patients with elevations of CK-MB had noninvasive cardiac evaluations. Four (7.7 percent) of the 52 patients had a rising and falling pattern of CK-MB that satisfied enzyme criteria of acute infarction. Three of these four also manifested classic echocardiographic features of right ventricular infarction. None of the four had evidence of left ventricular regional wall motion abnormalities or dysfunction. Of the 48 patients without elevations of CK-MB, only two had segmental right ventricular dysfunction. These findings suggest that pulmonary emboli can induce right ventricular infarction in some (7.7 percent) patients even when patients with a history of coronary artery disease and/or ECG changes of infarction are excluded. Conversely, the diagnosis of pulmonary embolism should be considered in patients when right ventricular infarction is diagnosed.

Adult↗

Disturbed atrioventricular electromechanical function long after Mustard operation for transposition of great arteries: a potential contributing factor to atrial flutter.

OBJECTIVE: The objectives were to study atrial and ventricular electromechanical function in patients long after Mustard repair for transposition of great arteries and to identify possible causes and physiologic disturbances in those with recurrent atrial flutter. METHODS: Electromechanical atrial and ventricular function was assessed in 22 patients (11 women) aged 27 +/- 5 years, 10 to 29 (mean 24) years after initial Mustard operation with electrocardiography and echocardiography. The study subjects involved 12 patients with documented atrial flutter and the remaining 10 without history of atrial arrhythmia served as controls. All patients were studied while in sinus rhythm. RESULTS: There was no difference in age, gender, or age at original Mustard surgery between the 2 patient groups. The P wave and QRS duration were significantly broader in patients compared with controls (128 +/- 14 ms vs 100 +/- 10 ms, P <.05 and 120 +/- 20 ms vs 93 +/- 6 ms, P <.01). Right ventricular end diastolic dimension was not different, whereas left ventricular fraction shortening was less (20% +/- 10% vs 35% +/- 12%, P <.01) in the patient group. Left and septal total ventricular long axes amplitude were significantly lower in patients compared with controls (1.4 +/- 0.4 cm vs 1.7 +/- 0.3 cm, P <.05 and 0.6 +/- 0.2 cm vs 1.0 +/- 0.3 cm, P <.01). Right-sided total long axis excursion was equally reduced in the 2 groups (1.0 +/- 0.3 cm). Septal and right-sided but not left-sided "a" wave was smaller in the patients (1.2 +/- 1 mm vs 3 +/- 1.2 mm, P <.001 and 1 +/- 1.3 mm vs 3 +/- 0.9 mm, P <.01). Right atrial electromechanical delay was significantly longer in patients with respect to controls (110 +/- 14 ms vs 84 +/- 25 ms, P <.001), but on the left there was no difference. The P wave duration correlated closely with right atrial electromechanical delay, r = 0.79, P <.003. Significant tricuspid regurgitation was found in 9 of 12 patients but none of the controls. CONCLUSION: Right ventricular dysfunction is present long after Mustard operation for transposition of great arteries whether flutter occurs. However, in patients with history of atrial flutter, evidence of left ventricular dysfunction, significant tricuspid regurgitation, impaired right atrial electrical and mechanical function, and reversed onset of atrial systole is also present. The consistent association of the disturbed atrial and ventricular electromechanical behavior suggests a multifactorial etiology for atrial arrhythmia.

Adult↗

Incidence of residual defects determining the clinical outcome after correction of tetralogy of Fallot: postoperative late follow-up.

The postoperative results in 150 patients who had repair of tetralogy of Fallot (mean follow-up, 10.2 +/- 2.6 years) were defined as good in 71.3%, fair in 20.7%, and unsatisfactory in 8.0% on the basis of clinical criteria. Ninety-six percent of the patients are socially active, 92.0% have a good exercise tolerance, and 79.3% participate in sports. Data from 78 postoperative hemodynamic studies show mild right ventricular dysfunction in almost all patients examined. Peak systolic right ventricular/left ventricular pressure ratio decreased in the postoperative period in 65.4% of patients, remained unchanged in 3.8%, and increased in 30.8%. Minimal residual anomalies can modify the prognosis substantially. Of our patients, 53.3% of those with a shunt (p less than 0.05), 37.5% of those with stenosis (not significant), and 53.8% of those with pulmonary incompetences (p = not significant) have fair or unsatisfactory results. The associated defects are particularly unfavorable. Rhythm and conduction disturbances have resulted in fair or unsatisfactory results in 65.1% of patients. Such a disturbance occurring soon after bypass must be considered an incremental risk factor: 52.9% of patients seen with rhythm and conduction disturbances show the same disturbances later (p less than 0.001).

Adolescent↗

Mechanisms of hypotension produced by platelet-activating factor.

Platelet-activating factor (PAF) is a phospholipid mediator that induces cardiovascular collapse and release of the secondary mediator thromboxane A2 (TxA2). To clarify mechanisms involved in this collapse and, specifically, the relative contribution of left ventricular and right ventricular dysfunction, we studied 12 open-chest pigs. PAF infusion (0.04-0.28 nmol.kg-1.min-1) induced a 5- to 120-fold increase in pulmonary vascular resistance, a 75-98% fall in cardiac output, and systemic arterial hypotension. Right ventricular failure was indicated by chamber enlargement, decreased shortening, and increased right atrial pressures. In contrast, left ventricular dysfunction was accompanied by decreases in chamber dimensions and filling pressures that were unresponsive to volume expansion. U 46619 (a stable TxA2 analogue) and mechanical pulmonary artery constriction induced changes similar to PAF. In 11 additional closed-chest pigs, TxA2 blockade with indomethacin attenuated the PAF-induced rise in pulmonary vascular resistance, right ventricular dysfunction, and systemic hypotension. A specific TxA2 synthase inhibitor, OKY-046, also diminished hemodynamic effects of PAF in six other pigs. Tachyphylaxis was not observed in five pigs repeatedly given PAF. We conclude that acute right ventricular failure as the result of severe increase in pulmonary vascular resistance is the primary mechanism early in the course of PAF-induced shock in the pig. PAF-induced release of TxA2 may contribute significantly to these events.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

Right ventricular function early after total or standard orthotopic heart transplantation.

Right ventricular failure after orthotopic heart transplantation (OHT) is classically related to preoperative pulmonary hypertension. However, the role of the enlarged atria in right ventricular dysfunction after OHT remains unclear. For that purpose, the right ventricular function in the first 2 days after OHT was compared in two groups of transplant recipients: 11 patients who underwent standard OHT (group I) and 9 patients who underwent total OHT, which consisted of total excision of both the left and right atria and OHT of an intact donor heart with its atria as well as its ventricle (group II). Right ventricular ejection fraction, cardiac index, and right-sided pressures were recorded at baseline and 4, 8, 12, 24, and 48 hours after OHT using a Swan-Ganz catheter with a rapid-response thermistor. Right ventricular function parameters did not differ between groups; they were characterized by a decrease in right ventricular ejection fraction and an increase in right ventricular end-diastolic volume index whereas cardiac index and right-sided pressures remained normal or slightly increased. Ischemic time (177 +/- 41 minutes in group I versus 178 +/- 39 minutes in group II) and preoperative pulmonary vascular resistance (1.9 +/- 0.7 Wood units in group I versus 3.0 +/- 1.5 Wood units in group II) were not different between groups. These results suggest that the anatomic and physiologic advantages offered by the modified technique of OHT had no clinical relevance in this group of patients with low preoperative pulmonary vascular resistances when compared with a group of patients who underwent transplantation with the standard technique.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Right ventricular myocardial infarction with anterior wall left ventricular infarction: an autopsy study.

Right ventricular myocardial infarction has been reported to occur exclusively in association with inferior left ventricular infarction. To determine the frequency of right ventricular myocardial infarction in association with anterior left ventricular myocardial infarction, all hearts with anterior myocardial infarction studied over a 3-year period were examined for evidence of right ventricular necrosis or scar. Of 97 hearts with anterior myocardial infarction, 13 (13%) had anterior right ventricular myocardial infarction. The right ventricular infarcts involved from 10% to 50% (mean 28%) of the circumference of the right ventricular free wall from base to apex. The associated left ventricular infarcts were all anteroseptal and large and involved from 36% to 67% (mean 50%) of the total area of the left ventricular free wall and septum. Nine of the 13 patients underwent equilibrium radionuclide angiography and six had demonstrable right ventricular regional and global dysfunction. Thus, right ventricular myocardial infarction does occur with anterior wall left ventricular infarction, and right ventricular dysfunction may be demonstrable by radionuclide angiography. Further investigation is needed to define the hemodynamic characteristics, clinical importance, and therapeutic implications of anterior right ventricular myocardial infarction.

Adult↗

Right ventricular dyssynchrony in patients with pulmonary hypertension is associated with disease severity and functional class.

BACKGROUND: Abnormalities in right ventricular function are known to occur in patients with pulmonary arterial hypertension. OBJECTIVE: Test the hypothesis that chronic elevation in pulmonary artery systolic pressure delays mechanical activation of the right ventricle, termed dyssynchrony, and is associated with both symptoms and right ventricular dysfunction. METHODS: Fifty-two patients (mean age 46 +/- 15 years, 24 patients with chronic pulmonary hypertension) were prospectively evaluated using several echocardiographic parameters to assess right ventricular size and function. In addition, tissue Doppler imaging was also obtained to assess longitudinal strain of the right ventricular wall, interventricular septum, and lateral wall of the left ventricle and examined with regards to right ventricular size and function as well as clinical variables. RESULTS: In this study, patients with chronic pulmonary hypertension had statistically different right ventricular fractional area change (35 +/- 13 percent), right ventricular end-systolic area (21 +/- 10 cm2), right ventricular Myocardial Performance Index (0.72 +/- 0.34), and Eccentricity Index (1.34 +/- 0.37) than individuals without pulmonary hypertension (51 +/- 5 percent, 9 +/- 2 cm2, 0.27 +/- 0.09, and 0.97 +/- 0.06, p < 0.005, respectively). Furthermore, peak longitudinal right ventricular wall strain in chronic pulmonary hypertension was also different -20.8 +/- 9.0 percent versus -28.0 +/- 4.1 percent, p < 0.01). Right ventricular dyssynchrony correlated very well with right ventricular end-systolic area (r = 0.79, p < 0.001) and Eccentricity Index (r = 0.83, p < 0.001). Furthermore, right ventricular dyssynchrony correlates with pulmonary hypertension severity index (p < 0.0001), World Health Organization class (p < 0.0001), and number of hospitalizations (p < 0.0001). CONCLUSION: Lower peak longitudinal right ventricular wall strain and significantly delayed time-to-peak strain values, consistent with right ventricular dyssynchrony, were found in a small heterogeneous group of patients with chronic pulmonary hypertension when compared to individuals without pulmonary hypertension. Furthermore, right ventricular dyssynchrony was associated with disease severity and compromised functional class.

Echocardiography↗

Risk factors for adverse short-term outcome in patients with pulmonary embolism.

Pulmonary embolism (PE) is a common and potentially fatal disease. Death usually occurs before hospital admission or in the initial in-hospital phase. A number of clinical and instrumental findings have been associated with a high risk of adverse short-term clinical outcomes in patients with PE. Advanced age, concomitant cardiopulmonary disease, and haemodynamic instability, as well as large perfusion defects at lung scanning and acute right heart dysfunction as assessed by echocardiography, are associated with adverse in-hospital outcome. Elevated serum levels of troponin I have been recently demonstrated to be associated with severe right ventricular dysfunction and adverse in-hospital outcome in patients with PE. Early recurrence of PE is associated with a high mortality rate. Right heart dysfunction, as assessed by echocardiography and an acute fall in platelet count, have been suggested as risk factors for recurrence of PE. A reduction in mortality in the subgroup of patients with a poor prognosis might be achieved by using more aggressive treatments such as thrombolysis and surgical or interventional procedures. However, such treatments are invariably associated with bleeding and other procedural complications.

Humans↗

Right ventricular failure: physiology and assessment.

Right ventricular function can be altered in several disease states involving lungs and heart. Severe right ventricular dysfunction is a major determinant of outcome in such situations, and may strongly influence clinical management. The complex geometry of the right ventricle and the different physiology with respect to the left ventricle make the right ventricular failure difficult to define and assess. The response to increased afterload is the main determinant of right ventricle physiology in pathologic conditions. This consists of right ventricular hypertrophy and enlargement, with reduced coronary blood flow to the right ventricular wall, dilation of tricuspid annulus and displacement of interventricular septum. This latter change involves the left ventricular diastolic function, which is reduced by leftward septal shifting. In right ventricle myocardial ischemia and infarction the primum movens of altered right ventricular function is not an increase in afterload, but the ischemic involvement of the right ventricle, more often in the setting of an inferior acute myocardial infarction. The assessment of right ventricular failure is based on thermodilution by pulmonary artery catheter, contrast and radionuclide ventriculography, echocardiography, and magnetic resonance. Among these techniques, thermodilution and echocardiography play a relevant role in clinical scenarios, being readily available and feasible bedside.

Heart Failure↗

Fatty infiltration of right ventricle (adipositas cordis): an unrecognized cause of early graft failure after cardiac transplantation.

Fatty infiltration of the right ventricle is usually an incidental finding at post-mortem, but may have clinical significance at times of physiologic stress. We report a case of fatal right ventricular dysfunction immediately after cardiac transplantation secondary to massive fatty infiltration of the donor right ventricle. Ante-mortem diagnosis of fatty infiltration may be difficult to determine despite non-invasive cardiac evaluation. If the diagnosis of fatty infiltration is suspected at time of donor harvest, the relative risks and benefits of proceeding with transplantation should be carefully assessed.

Adipose Tissue↗

[Extracardiac causes of right ventricular insufficiency].

Evidence for manifest right ventricular dysfunction is considered a critical threshold in the development of a fatal event after acute pulmonary embolism. While the acute event impressively reflects the clinical significance of right ventricular function, various disorders such as idiopathic pulmonary arterial hypertension, secondary pulmonary hypertension in lung diseases, carcinoid heart disease, and portopulmonary hypertension can lead to chronic right ventricular failure. Adapted treatment makes it possible to alleviate the patients' distress and presumably also improve the prognosis. The clinical picture of right ventricular insufficiency can also be imitated in constrictive or adhesive pericarditis and pericardial tamponade. Pericardiocentesis of the tamponade provides initial hemodynamic improvement. Causal treatment is based on cytological findings and/or results of epicardial or pericardial biopsy to classify malignant and nonmalignant effusions. Cardiac surgery with pericardiolysis and (partial) pericardial resection remains the method of choice for symptomatic constrictive pericarditis.

Acute Disease↗

Incidence of right ventricular asynergy in patients with coronary artery disease.

The effects of coronary artery disease on patterns of left ventricular contractility have been thoroughly investigated. In contrast, little is known about the incidence of right ventricular dysfunction induced by this disease. To evaluate the frequency of right ventricular asynergy, biplane right ventricular cineangiograms were obtained in 26 patients. Seven segmental axes of shortening were analyzed in each end-systolic and end-diastolic frame and normalized as percent decrease (or increase) in axis from end-diastolic length. Of 26 patients, 8 (Group I) served as normal (control) subjects. The remaining 18 patients had significant coronary artery disease; 6 of these (Group II) had no significant disease of the right coronary artery, whereas 12 (Group III) had significant obstruction of this artery. Four patients in Group II had a previous anteroseptal myocardial infarction, and six in Group III had a previous inferior myocardial infarction. There was a progressive decrease in segmental axes of shortening from Group I to II and from Group II to II, but the decrease was not significant at the level P less than 0.01. Only one patient in Group II had frank dyskinetic segmental motion of the interventricular septum (this patient had had a previous anteroseptal myocardial infarction), whereas two patients in Group III had dyskinetic segmental motion of the free right ventricular wall (both had previous inferior myocardial infarction). Therefore, coronary artery disease seldom produces significant right ventricular asynergy. Abnormal septal motion is associated with previous anteroseptal myocardial infarction; however, dyskinetic motion of the free right ventricular wall occurs only in patients with a right coronary arterial lesion and previous inferior myocardial infarction.

Angiocardiography↗

Vitamin K reduces bleeding in left ventricular assist device recipients.

BACKGROUND: Despite advances in left ventricular assist device (LVAD) design that permit support without anticoagulation, LVAD recipients often suffer profound bleeding complications. This bleeding diathesis may be attributable to pre-operative right-ventricular failure with concomitant hepatic dysfunction. The purpose of this study was to characterize coagulation abnormalities in LVAD recipients and determine the impact of pre-operative vitamin K administration on the incidence of postoperative bleeding. METHODS: Hemostatic and liver function profiles were obtained in 66 recipients of the Heartmate LVAD; 39 of these patients received perioperative vitamin K. RESULTS: During LVAD support, hepatic synthetic function improved as evidenced by increases in clotting factors II, V, VII, XI. There was ongoing fibrinolysis with elevation of fibrinopeptide A and D-dimers and diminution of fibrinogen; however, plasminogen levels did not decline suggesting that systemic disseminated intravascular coagulation (DIC) did not occur. Bleeding requiring re-exploration more than 48 hours postimplantation occurred in 9 of 66 patients (13.6%). Prior to implantation, patients that bled had decreased levels of factor II (52.2 +/- 27.1% vs 69.7 +/- 26.6%; p = 0.048) and prolonged prothrombin times (16.5 +/- 2.4 seconds vs 13.8 +/- 3.1 seconds; p = 0.005) compared to patients that did not bleed. Seven of 27 patients (25.9%) not treated with vitamin K bled, while only 2 of 39 (5.1%) patients treated with vitamin K required re-exploration for bleeding (p = 0.026). CONCLUSIONS: We conclude that: (1) Liver synthetic function improves during LVAD support resulting in increased levels of circulating coagulation factors; (2) ongoing fibrinolysis occurs but likely only represents remodeling of fibrin on the LVAD surface; (3) perioperative vitamin K reduces nonsurgical bleeding in LVAD recipients.

Disseminated Intravascular Coagulation↗

[Can irreversible ventricular dysfunction be identified in patients with heart valve disease?].

Cardiologists and heart surgeons are often faced with the problem of the optimal therapeutic indication in patients with valvular heart disease presenting with severe myocardial dysfunction, as it is difficult to evaluate the degree of reversibility of a severe alteration of ventricular function in these patients. Myocardial dysfunction is often multifactorial in patients with valvular heart disease and the role of myocardial ischaemia secondary to associated coronary heart disease must not be neglected. On the other hand, the compensatory capacity of the myocardium varies from one patient to another ("constitutional" myocardial factor or related to the aetiology of the valvular heart disease?). Although the methods of investigation of myocardial function currently available are able to precisely evaluate the degree of severity of myocardial dysfunction, they are unable to accurately predict the degree of reversibility. 1. In pure mitral stenosis, severe left ventricular dysfunction is very rare; more or less rapidly, pulmonary hypertension induces slowly progressive right ventricular dysfunction which remains reversible for a long time. 2. In mitral incompetence, left ventricular systolic function is correctly evaluated by the ejection fraction (LVEF). There is a high risk of irreversible left ventricular dysfunction in operated patients with an LVEF of less than 0.40. In these patients, left ventricular function is slightly improved after mitral repair, while LVEF decreases after mitral valve replacement. The combined study of right ventricular systolic function is useful in patients with mitral disease, as this function may be insidiously altered and the presence of right heart failure, regardless of its cause, considerably increases the late postoperative mortality of mitral valve disease. 3. In aortic stenosis, left ventricular dysfunction, hypertrophy and interstitial fibrosis remain reversible for a long time. Severe alteration of LV function therefore does not exclude the possibility of very good postoperative recovery. However, this is improbable in the presence of: a very marked increase in LV mass and/or end-systolic volume, and/or inoperable associated coronary artery disease, and/or the combination of low ejection fraction, severely decreased cardiac output, and low transvalvular gradient (not increased by cautious dobutamine infusion), and/or clinical signs of complete heart failure. 4. In aortic incompetence, progressive alteration of left ventricular function, often asymptomatic, is reflected by the increased dimensions of the LV and a reduction of the fraction of ejection. The reversibility of LV dysfunction is difficult for evaluate. The long clinical course of this dysfunction is one of the most reliable predictors of irreversibility, together with a fall in the resting isotope LVEF.(ABSTRACT TRUNCATED AT 250 WORDS)

Aortic Valve↗