Left ventricular volume reduction for end-stage heart disease

Partial left ventriculectomy (PLV) was recently introduced for end-stage dilated cardiomyopathy to improve ventricular function. Since November 1996 we have performed PLV in 14 patients; preoperatively 4 patients had idiopathic dilated cardiomyopathy and 10 had ischemic dilated cardiomyopathy. 57.1% of patients were in New York Heart Association functional Class IV. The mitral valve was replaced in 11 patients. Postoperative echocardiography showed a reduction of left end-diastolic diameter (55.4 +/- 5.4 mm) and an increase in forward ejection (cardiac index from 2.19 +/- 0.571 min/m2 to 2.67 +/- 0.931/min/m2). The 30-day mortality was 28.6% and 20-month survival was 57.2%. Only one patient was not in NYHA functional class due to postoperative progressive mitral incompetence. Prognostic factors should be identified to avoid early failure. However, even if the mortality rate for PLV high, this operation is a valid choice for the treatment of end-stage dilated cardiomyopathy.     

Left ventricular volume reduction and reconstruction in ischemic cardiomyopathy

Abstract Background: Ischemic cardiomyopathy can be the result of large or small my-ocardial infarctions or due to myocardial hibernation. Patients with an end-systolic volume index >100 mL/m² do not benefit from revascularization alone and require an operation that reduces ventricular volume. Various approaches to reduce ventricular volume have been described. We applied several of these techniques in patients with end-stage ischemic cardiomyopathy. Methods: Forty eight patients with end-stage ischemic cardiomyopathy (Class III-IV) underwent left ventricular volume reduction operations with coronary revascularization and mitral valve repair or Alfieri valvoplasty. Fourteen patients underwent interpapil-lary resections, 22 anterior resections, 4 posterior resections, 2 anterior and posterior resections, and 6 patients reduction of left ventricular volume with endocavitary patches. Results: All the techniques used improved left ventricular function. Analysis of mortality revealed that extensive resections (interpapillary, anterior, and posterior resection) had a 43% mortality. However, a limited resection or a ventricular reconstruction with an endocavitary patch had only a 12.5% mortality. When we changed our approach to a more conservative one, mortality was reduced from 26% the first 12 months to 13% in the last 15 months of the study. Conclusions: Ischemic cardiomyopathy has a poor prognosis if the end-systolic volume index exceeds 100 mL/m². Various procedures exist to reduce left ventricular volume. Extensive ventricular resections improve ventricular function, but have a high mortality. This led us to use other methods of ventricular volume reduction such as more conservative resections combined with left ventricular reconstructions or ventricular volume reduction with endocavitary patches. Mortality was reduced significantly by this approach. The patients that survived have remained Class I-II in a follow-up that extends up to 30 months. Surgical therapy of Class III-IV ischemic cardiomyopathy is feasible, but aggressive ventricular resections have a high mortality. We advocate a more reconstructive approach with limited or no ventricular resection.     

Left ventricular volume reduction surgery for heart failure: a physiologic perspective

BACKGROUND: Ventricular volume reduction surgery for idiopathic cardiomyopathy fails to improve cardiac output and is associated with a high incidence of recurrent heart failure. Volume reduction surgery achieved by removing akinetic or dyskinetic myocardium after myocardial infarction appears to be associated with better outcomes. The reasons for the differences in outcomes are not clear. METHODS AND RESULTS: The hemodynamic effect of the major forms of volume reduction surgery were predicted by using a composite model of the left ventricle in which 20% of the myocardium was given properties of either weak but contracting muscle, an akinetic scar, or a dyskinetic scar (aneurysm). The end-systolic and end-diastolic pressure-volume relationships were determined numerically for each simulated operation. Any volume reduction procedure reduced chamber size, shifting end-systolic and end-diastolic pressure-volume relationships leftward. With resection of weak but contracting muscle, the leftward shift was greater for the end-diastolic than for the end-systolic pressure-volume relationship. Conversely, with resection of dyskinetic scar, the leftward shift was greater for end-systolic than for end-diastolic pressure-volume relationships. In contrast, resection of stiff scar shifted the 2 relationships equally. The effect on overall pump function was indexed by the relationship between total ventricular mechanical work and end-diastolic pressure. There was a beneficial effect on this relationship of resecting dyskinetic tissue, an equivocal effect of akinetic scar resection, and a negative effect of removing contracting myocardium. CONCLUSIONS: The effect of volume reduction surgery on overall ventricular pumping characteristics is determined by the differential effects on end-systolic and end-diastolic properties, which in turn are determined by the material properties of the region being removed.     

Left ventricular volume reduction surgery: The 4th International Registry Report 2004

BACKGROUND AND METHODS: An international registry of left ventricular volume reduction (LVVR) procedures, including partial left ventriculectomy, has been expanded, updated, and refined to include 568 cases voluntarily reported from 52 hospitals in 12 countries. RESULTS: Gender, age, ventricular dimension, ethnology, myocardial mass, presence or absence of mitral regurgitation, as well as transplant indication, had little effect on event-free survival, which was defined as either absence of death or ventricular failure requiring mechanical assist or transplantation. Poor preoperative patient condition such as New York Heart Association classification IV, depressed contractility and decompensation requiring an emergency procedure were associated with reduced event-free survival. Other risk factors included an early surgery date, lack of experience, dilated cardiomyopathy as the underlying pathology and extended myocardial resection. Performance of LVVR reached a peak by 1998, but was largely abandoned by 2001, except in Asia, where experienced institutes continue to perform it in patients in better condition with preserved myocardial contractility. CONCLUSION: Avoidance of risk factors appears to have contributed to the recent survival improvement and may help stratify patients for LVVR. While performance has been decreasing, the concept has been extended to other LVVR and less invasive procedures, which are now under clinical trials.     

Left ventricular reduction in a Jehovah's Witness

For Jehovah's Witnesses with severe heart failure, left ventricular reduction surgery may be a satisfactory alternative to cardiac transplantation. Compared with transplantation, left ventricular reduction surgery can involve less blood loss thus decreasing the need for blood-volume replacement. More importantly, left ventricular reduction surgery obviates the need for a donor organ.     

Late ventricular structure after partial left ventriculectomy

Nine months after partial ventriculectomy, a 53-year-old man died of progressive heart failure. His heart was examined to determine the alignment of the muscle fibers around the ventricular scar, which was 11 cm long, 1.3 cm thick and 4 cm wide. The scar reached 2 to 12 mm beyond the surgical suture line. The fibers in the middle and subendocardial layers were malaligned, resulting in convergence, compression and regional necrosis.     

Perioperative care in left ventricular volume reduction

BACKGROUND: While the operative technique of left ventricular volume reduction (LVVR) is rapidly becoming standardized, the optimal perioperative management strategy is yet to be determined. We present our experience with the care of patients undergoing LVVR. METHODS: LVVR was performed in 21 patients (mean age = 65.5 years) with congestive heart failure. Our management strategy was initially based on afterload reduction with sodium nitroprusside, but was later modified to include routine preoperative intra-aortic balloon support, normothermic cardiopulmonary bypass, antegrade intermittent warm blood cardioplegia, and postoperative support with phosphodiesterase-III inhibitors. Hemodynamic manipulations are aimed to attain systemic vascular resistance between 600 and 800 dyne/sec per cm(-5) and the lowest mean blood pressure that is able to maintain satisfactory systemic perfusion. Postoperatively, aggressive antifailure medical therapy with a high dose of angiotensin converting enzyme inhibitors, nitrates, and diuretics was initiated early and maintained indefinitely. RESULTS: Using this approach, postoperative progress was characterized by hemodynamic stability. IABP support was used for 59.6+/-9 hours following surgery, and inotropic support for 103+/-12 hours. In our series there were four (19%) in-hospital deaths, two of which were related to heart failure. CONCLUSION: The described approach is associated with an acceptable early outcome. However, further advances in myocardial protection methods and pharmacological and mechanical support techniques are necessary for a wider adoption of this procedure.     

An alternative to left ventricular volume reduction.

BACKGROUND: Left ventricular (LV) remodeling leading to ventricular dilatation is ultimately a maladaptative process according to the law of Laplace. To counteract the wall stress increase, a new concept of reducing the LV cavity radius by changing the LV globular shape to a bilobular one through the insertion of transventricular splints has emerged. This procedure is tested in a model of congestive heart failure. METHODS: A bovine model was used (n = 9). Following splint insertion through a sternotomy, boluses of 2 liters of crystalloid were injected. After every bolus, hemodynamic measurements were performed without and with the splints tightened to a 10% and 20% stress level reduction, respectively. Comparisons between the 3 measurements were performed with analysis of variance test (p < 0.05). RESULTS: Splint tightening significantly reduced right and left heart pressures for central venous pressure (CVP) >10 mm Hg (CVP: 14.7 +/- 5.2, 12.1 +/- 5, 10.6 +/- 4.7 mm Hg, p < 0.001 for baseline, 10% and 20% stress level reduction, respectively; mean pulmonary artery pressure: 33.5 +/- 4.7, 31 +/- 4.4, 29.4 +/- 5.1 mm Hg, p < 0.001; pulmonary capillary wedge pressure: 20.5 +/- 2.8, 18.9 +/- 3.3, 17.5 +/- 3.1 mm Hg, p < 0.001). The same holds true for cardiac output (6.5 +/- 1.6, 6.7 +/- 1.4, 6.8 +/- 1.7 liter/minute, p < 0.001), whereas heart rate and mean arterial pressure were not affected. The systemic and pulmonary resistances did not vary significantly throughout the procedure. Importantly, none of the hemodynamic parameters worsened at any stage with the splints. CONCLUSIONS: In this model, hemodynamic parameters are improved with the splints for higher values of CVP, supporting the concept of reshaping the remodeled LV. This technique has the potential to improve patients with congestive heart failure.     

Left ventricular adaptation to volume overload from large aortocaval fistula

The manner in which the left ventricle responds to an acute volume overload has not been well defined. Left ventricular performance was studied in six chronically instrumented resting awake dogs in the control state and serially after creation of a large abdominal aortocaval shunt. Ultrasonic transducers measured minor and major axis diameters and equatorial wall thickness. Left ventricular pressure was obtained with micromanometers. Cardiac contractility was evaluated by the load-independent contractility index, EMAXsc (slope of the normalized end-systolic equatorial midwall circumferential stress-equatorial midwall circumference relationship). By 1 week postshunt, the dog had clinical signs of congestive heart failure (ascites, dyspnea, limb edema); although systolic aortic pressure remained stable, heart rate, end-diastolic volume, pulse pressure (systolic minus diastolic pressure), cardiac output, minute work and dp/dtmax were significantly increased. At 1 week the calculated left ventricular mass was increased by 10.1% +/- 4.0% above control. EMAXsc was significantly increased immediately after shunting but returned to control at 1 day and was less than control at 1 week. Thus adaptation of the left ventricle to acute volume overload is characterized by use of inotropic, chronotropic, and Starling reserves. However, chronic volume overload is characterized by decreased inotropic state and an apparent increase in hemodynamic performance (dp/dtmax, cardiac output, minute work), which appears to be maintained by an increase in cardiac mass and by chronotropic and Starling reserves.     

Left ventricular hydatid cyst causing acute pericardial tamponade without rupture

Indian Journal of Thoracic and Cardiovascular Surgery -     

Left ventricular pressure and volume unloading during pulsatile versus nonpulsatile left ventricular assist device support

BACKGROUND: Nonpulsatile axial or centrifugal pumps are the latest generation of left ventricular assist devices (LVAD). Whether left ventricular (LV) unloading and outcome in these devices is similar to pulsatile LVADs during long-term support has not been investigated. We compared LV unloading and mortality between different types of LVAD support (pulsatile versus nonpulsatile). METHODS: In 31 patients undergoing long-term LVAD implantation (nonpulsatile = 10, pulsatile = 21) preoperative and postoperative echocardiographic and hemodynamic assessment with right heart catheterization had been obtained. RESULTS: All patients had similar echocardiographic, hemodynamic, and clinical heart failure characteristics at baseline. The degree of LV pressure unloading was the same in both device types, caused by similar reduction of mean pulmonary pressure (18.6 +/- 5.1 versus 18.3 +/- 7.5 mm Hg) and pulmonary capillary wedge pressure (8.9 +/- 4.4 versus 8.0 +/- 7.0 mm Hg). Left ventricular volume unloading was pronounced with a pulsatile device owing to a statistically significant higher pump output (5.1 +/- 1.0 L/min) in comparison with nonpulsatile LVADs (3.6 +/- 0.9 L/min, p < 0.001). Echocardiographic-determined end-systolic indicators confirm this augmentation in pulsatile LVADs. Etiology or the time interval of hemodynamic reassessment had no impact in left ventricular pressure unloading, but LV volume unloading decreased between day 60 and 120 in patients with nonpulsatile LVADs. The preoperative and postoperative transplant mortality was comparable in both groups. CONCLUSIONS: Left ventricular pressure unloading is similar in patients with nonpulsatile as compared with pulsatile implantable long-term assist devices. Left ventricular volume unloading is pronounced in pulsatile LVADs.     

Left ventricular end-diastolic volume from ejection fraction and stroke volume in pigs during IVC occlusion

BACKGROUND: Real-time measurement of left ventricular end-diastolic volume (LVEDV), combined with left ventricular end-diastolic pressure (LVEDP), would allow continuous measurement of intraoperative diastolic function. In pursuit of this goal, we examined stroke volume divided by ejection fraction for calculation of LVEDV(sv/ef). METHODS: Five anesthetized pigs underwent median sternotomy and pericardiotomy. A transit-time ultrasonic flow probe on the ascending aorta provided cardiac output. A micromanometer provided LV end-diastolic pressure. End-diastolic and end-systolic areas were measured from LV short-axis cross sections to obtain ejection fraction. LVEDV(sv/ef) was calculated during IVC occlusion. Steady-state LVEDV(echo) was determined using a three-plane echocardiography model. LVEDV(echo) was used to validate steady-state LVEDA in each experiment. RESULTS: Correlation coefficients for linear and pressure-volume relation analyses ranged from 0.46 to 0.99. The two methods for measuring LVEDV generated compliance curves with an overall reliability coefficient of 0.84. CONCLUSIONS: The LVEDV(sv/ef) method may facilitate real-time determination of LV compliance.     

Early experience with left ventricular volume reduction surgery in Syria

OBJECTIVE: To review our early experience with left ventricular volume reduction surgery (the Batista operation) in the management of patients with end-stage heart failure. METHODS: Between December 1996 and April 1998, 10 patients (9 males, mean age 32yr) with advanced symptomatic cardiomyopathy underwent left ventricular volume reduction surgery at Damascus University Cardiovascular Surgical Center. The cause of cardiomyopathy was idiopathic in three patients, valvular in four, ischemic in two, and viral myocarditis in one patient. Concomitant procedures included aortic valve replacement in four patients, mitral valve repair in six patients, and coronary artery bypass grafting in two patients. RESULTS: All patients survived the procedure. Echocardiography prior to discharge documented significant improvement in ejection fraction in all but two patients. Mean follow-up was 7.6 months. After discharge, three patients developed progressive congestive heart failure to which they subsequently succumbed, and two more patients died suddenly late postoperatively. Only two patients continue to show both clinical and echocardiographic evidence of improvement. CONCLUSION: Left ventricular volume reduction surgery cannot be freely advocated until better means are found to identify patients who will benefit from the procedure, and proper prophylaxis against fatal postoperative complications can be afforded.     

Left ventricular ejection fraction, end–diastolic volume and endsystolic volume during induction of anaesthesia

Abstract: Left ventricular ejection fraction, end–diastolic volume and end–systolic volume were determined in 74 patients with ischaemic heart disease (IHD), during induction of anaesthesia, using different anaesthetic techniques. Ejection fraction measured with nuclear angiocardiography (Nuclear Stethoscope), was combined with stroke volume, determined with thermodi–lution, to calculate end–diastolic volume and end–systolic volume. Together with pressure measurements, the left ventricular pressure–volume relationship in end–distole and end–systole could be evaluated. Left ventricular diameter, determined with transthoracic 2D echocardiography, was subsequently studied during induction of anaesthesia in 11 patients with IHD. The results from this study were compared with the findings of previous studies. In a further study the relationship between pressure readings in the ascending aorta and the radial artery was investigated during anaesthesia in 26 patients with IHD. Special reference was made to the relationship between aortic and radial artery dicrotic notch pressure. Conclusions: 1. Induction of anaesthesia with hypnotics, low dose fentanyl and pancuronium caused a considerable decrease in left ventricular preload, estimated as end–diastolic volume (I, III, V). 2. Induction of anaesthesia with isoflurane and nitrous oxide in combination with hypnotics, low dose fentanyl and pancuronium, caused a similar reduction in preload (II). 3. The decrease in preload, during induction of anaesthesia with the low dose fentanyl techniques, was of the same magnitude (31–45%), despite the use of several different drug combinations (I, II, III, V). 4. In addition to the decrease in end–diastolic volume, there was a decrease in end–systolic volume during induction of anaesthesia in the low dose fentanyl groups. The net result was an increase in ejection fraction and a decrease in stroke volume (I, II, III). 5. Laryngoscopy and intubation caused a decrease in left ventricular ejection fraction and an increase in end–diastolic and end–systolic volume in the low dose fentanyl groups (I, II, III). 6. Nitroglycerin as an iv bolus effectively prevented the decrease in ejection fraction and the increase in end–diastolic and end–systolic volume during laryngoscopy and intubation, during induction of anaesthesia with a low dose fentanyl technique (III). 7. Left ventricular filling pressure was poorly correlated to left ventricular enddiastolic volume (I, II, III). 8. A high dose fentanyl technique in combination with pancuronium implied stable haemodynamics, with reference to left ventricular ejection fraction, enddiastolic volume and end–systolic volume, during induction of anaesthesia including laryngoscopy and intubation (I). 9. Left ventricular end–systolic pressure, measured as the dicrotic notch pressure in the ascending aorta, could be estimated from pressure measurements in the radial artery, with reasonable accuracy, in the period immediatley preceding cardio–pulmonary bypass (IV). 10. The estimated changes in left ventricular end–diastolic and end–systolic volume, during induction of anaesthesia, were similar using two different techniques of measurement: therrnodilution in combination with nuclear angiocardiography (I, II, III) and transthoracic echocardiography (V).     

Left ventricular global and regional function during lumbar epidural anesthesia in patients with and without angina pectoris. Influence of volume loading

The influence of lumbar epidural anesthesia without cardiac sympathectomy on global and regional left ventricular function was investigated prior to surgery in eight normal subjects (group 1) and in ten patients suffering from stable mild effort-related angina (group 2). In both groups, epidural blockade was performed with 10 ml 0.5% plain bupivacaine. To differentiate the effects due to epidural blockade from those related to volume expansion, three sets of measurements were obtained: control, epidural blockade without volume loading, and epidural blockade with volume loading (500 ml lactated Ringer's solution). Radionuclide angiography was used to determine cardiac output, left ventricular ejection fraction, end systolic and end diastolic volumes, and to analyse left ventricular wall motion. Peak systolic pressure-end systolic volume ratio was used as an index of myocardial contractility. Seventy-two hours postoperatively, a thallium 201 myocardial scintigraphy obtained after iv dipyridamole detected myocardial defects in all patients with a history of angina. These defects were fully redistributed in eight out of ten patients. Throughout the procedure, patients with a history of angina exhibited neither chest pain nor ECG evidence of myocardial ischemia. At control, left ventricular ejection fraction (LVEF) and systolic pressure-volume ratio (SPVR) were lower in group 2 than in group 1 (LVEF: 0.54 +/- 0.02 vs. 0.64 +/- 0.02, P less than 0.01), (SPVR: 2.3 +/- 0.2 vs. 3.3 +/- 0.4 mmHg/ml, P less than 0.05). In addition, 19 hypokinetic sectors were found in group 2.(ABSTRACT TRUNCATED AT 250 WORDS)     

Beta-blockade by sotalol in early myocardial infarction decreases ventricular arrhythmias without increasing left ventricular volume

Although early beta-blockade in acute myocardial infarction (AMI) may have potential benefits owing to an anti-arrhythmic effect and limitation of infarct size, the haemodynamic effects are not well characterised. Accordingly, we studied the effects of intravenous beta-blockade by sotalol in AMI, commencing a mean of 6 hours after the onset of chest pain, with particular reference to systemic haemodynamic changes and left ventricular (LV) volumes. Thirty patients were randomised to a control group or to sotalol therapy starting with 40 mg and increasing to 120 mg, followed by the maximal dose tolerated every 6 hours for 72 hours. Sotalol reduced heart rate and mean blood pressure without elevating pulmonary wedge pressure or increasing enzymatic infarct size. Sotalol also decreased the incidence of ventricular tachycardia (P less than 0.001). An important new finding was that there was no increase in the LV volume measured by radionuclide techniques. Therefore intravenous sotalol safely achieved its beneficial effects without causing LV dilatation.     

Left ventricular hemangioma

Cardiac hemangiomas are quite rare benign tumors of vascular origin often detected incidentally during routine examinations. Here we present the diagnostic evaluation and excisional biopsy of such a cardiac tumor in a 20-year-old man.     

Left ventricular aneurysm

Left ventricular aneurysm in African patients is most often luetic; the only other common left ventricular aneurysm in African patients is agnogenic and not a complication of coronary artery disease. The management of a left ventricular aneurysm by surgical excision with cardiorespiratory bypass in an African patient is described. The literature which relates to left ventricular aneurysm in African patients is briefly reviewed.