PubMed Health⌕ Search

Biomedical subjects

M A Acker

Publications and source records attributed to M A Acker.

At least 19 recordsLinked to original sources
PubMed2001

Mechanical circulatory support for patients with acute-fulminant myocarditis.

This report provides a review of mechanical circulatory support for patients in cardiogenic shock secondary to acute/fulminant myocarditis. Experience and outcomes with extracorporeal membrane oxygenation, left ventricular assist device support (ABIOMED, Thoratec, Thermo Cardiosystems, Novacor), and biventricular ventricular assist device support (ABIOMED, Thoratec) are described. Patients in cardiogenic shock secondary to acute myocarditis in its fulminant presentation can recover, surprisingly with normal cardiac function. An aggressive approach to the use of mechanical support is strongly justified. Survival, either by bridge to transplant or recovery, should approach 70%. Transplantation can often be avoided.

Acute Disease↗
PubMed2001

Mechanical circulatory support for acute heart failure.

Circulatory support devices are frequently required in postcardiotomy shock, postmyocardial infarction shock, and acute myocarditis. A panel of cardiac surgeons addressed the use of these devices in 4 patients. Cardiogenic shock after mitral valve replacement was considered best served by a left ventricular assist device (VAD) with apical rather than atrial cannulation. A left VAD should be placed first and a right VAD only if needed. Acute myocardial infarction shock was considered best treated with a left VAD with left ventricular cannulation to avoid thrombosis. If cardiac transplantation is an option, a long-term device must be considered. Young patients with acute fulminant myocarditis should be implanted with VADs in anticipation of recovery, and transplantation should be delayed. Patients with severe heart failure after coronary bypass grafting were considered best served by an extracorporal membrane oxygenation (ECMO) system or a VAD. Current postcardiotomy survival rates of postcardiotomy patients of 20% to 40% are worthwhile, but can be improved. Temporary devices such as ECMO can be changed to more long-term devices when necessary.

Acute Disease↗
PubMed2001

Application of "double bridge mechanical" resuscitation for profound cardiogenic shock leading to cardiac transplantation.

BACKGROUND: In patients with acute profound cardiogenic circulatory failure unresponsive to conventional resuscitation, we instituted immediate aggressive application of extracorporeal membrane oxygenation (ECMO) to restore circulatory stability. Long-term hemodynamic support was accomplished with an early "bridge" to ventricular assist device (VAD) before definitive treatment with cardiac transplantation. METHODS: A respective review of ECMO and VAD data registries was instituted. RESULTS: From May 1996 to July 2000, 23 patients were placed on ECMO support for profound cardiogenic circulatory failure. Eleven patients (47%) were withdrawn from support due to severe neurologic injury or multisystem organ failure. Three patients (13%) were weaned off ECMO with good outcome. Nine patients (39%) were transferred to a VAD. Two patients expired while on VAD support, and 7 of the VAD-supported patients (78%) survived to transplantation. Overall survival was 43%. CONCLUSIONS: Emergent ECMO support is a salvage approach for cardiac resuscitation once conventional measures have failed. In neurologically intact patients, the early transfer to a VAD quickly stabilizes hemodynamics, avoids complications, and is essential for long-term circulatory support before definitive treatment with cardiac transplantation.

Adolescent↗
PubMed2000

Frequency, risk factors, and clinical outcomes of left ventricular assist device-associated ventricular thrombus.

A retrospective, transesophageal study of 51 consecutive patients receiving a left ventricular (LV) assist device (AD) over a 2-year period showed that LVAD-associated LV thrombosis (16%) was predicted by acute myocardial infarction, atrial cannulation, and postimplantation bleeding, and was associated with a fourfold increased risk of stroke compared with patients without thrombosis. LV cannulation, when using short-term LVADs, may decrease the incidence of LV thrombosis, and early transition to Heartmate-LVAD support may improve outcome.

Aged↗
PubMed2000

Detection of anti-HLA antibody by flow cytometry in patients with a left ventricular assist device is associated with early rejection following heart transplantation.

BACKGROUND: Patients with a left ventricular assist device (LVAD) as a bridge to heart transplantation (HT) often have elevated levels of panel reactive antibodies (PRA). The clinical significance of anti-human histocompatibility leukocyte antigen (HLA) antibodies detected by flow cytometry in PRA negative patients remains unclear. METHODS: Eighteen patients who underwent LVAD placement as a successful bridge to HT had standard anti-human globulin complement-dependent cytotoxicity and retrospective flow cytometry assays performed to detect class I anti-HLA antibodies. A positive flow result was defined as a fluorescent ratio of 23:1 versus a negative control. RESULTS: Six patients had anti-HLA antibodies detected by flow cytometry. Univariate analysis demonstrated more moderate-severe rejection episodes (ISHLT > or = IIIA) at 2 months (0.83+/-0.75 vs. 0; P=0.04) and a trend toward decreased time to first rejection (61+/-17 vs. 225+/-62 days; P=0.06) in these patients. No differences were observed in donor-recipient HLA mismatch or 1 year Kaplan-Meier survival between patients with or without anti-HLA antibodies. CONCLUSION: Despite a negative PRA, LVAD patients with class I anti-HLA antibodies detected by flow cytometry have a greater incidence of moderate-severe rejection in the first 2 months after HT. Flow cytometry may be a useful clinical tool in screening PRA negative LVAD patients before transplantation. Patients with positive anti-HLA antibody screening by flow cytometry may require more intensive immunosuppression in the early post-HT period.

Adult↗
PubMed2000

Changes in lipoprotein(a) concentration after orthotopic heart transplantation.

BACKGROUND: Elevated concentrations of lipoprotein(a) have been considered an important risk factor in the development of premature cardiovascular disease and have been proposed as a risk factor in the development of accelerated cardiac allograft vasculopathy after orthotopic heart transplantation. METHODS: We prospectively measured lipoprotein(a), fasting cholesterol, and triglyceride concentrations before (n = 38), 6 months (n = 38), and 1 year (n = 21) after orthotopic heart transplantation. The mean age of the patients was 52 +/- 2 years. Eighty-seven percent of the patients were men, 82% were white, and 61% had ischemic cardiomyopathy. RESULTS: Mean lipoprotein(a) concentration was lower 6 months after transplantation than it was before the operation (23 +/- 3 mg/dL vs 17 +/- 3 mg/dL; P =.014) and remained low 1 year after transplantation (23 +/- 3 mg/dL vs 18 +/- 4 mg/dL; P = not significant). In contrast, mean cholesterol concentration was higher 6 months after transplantation (171 +/- 8 mg/dL vs 221 +/- 8 mg/dL; P <.001) and 1 year (171 +/- 8 mg/dL vs 205 +/- 10 mg/dL; P <.01) than it was before transplantation. Triglyceride concentration was higher 1 year after transplantation than it was before the operation (146 +/- 13 mg/dL vs 184 +/- 20 mg/dL; P =.017). CONCLUSIONS: Lipoprotein(a) concentrations decrease during the 6 months after transplantation and stay low for at least 1 year after the operation. Additional studies are needed to ascertain the effect these changes in lipoprotein(a) concentration on the development of cardiac allograft vasculopathy.

Adolescent↗
PubMed2000

Ten weeks of rapid ventricular pacing creates a long-term model of left ventricular dysfunction.

OBJECTIVE: Rapid ventricular pacing produces a reliable model of heart failure. Cessation after 4 weeks of rapid ventricular pacing results in rapid normalization of left ventricular function, but the left ventricle remains persistently dilated. We present novel data that show that prolonged rapid ventricular pacing (10 weeks) creates a model of chronic left ventricular dysfunction. METHODS: In 9 dogs undergoing 10 weeks of rapid ventricular pacing, left ventricular function and volumes were serially assessed by using 2-dimensional echocardiography and pressure-volume analysis for 12 weeks after cessation of pacing. RESULTS: Increased end-diastolic volume and decreased systolic and diastolic function were seen at the end of pacing. By 2 weeks of recovery from rapid ventricular pacing, end-diastolic volume and ejection fraction were partially recovered but did not improve further thereafter. Load-independent and load-sensitive indices of function obtained by pressure-volume analysis at 8 and 12 weeks of recovery confirmed a persistence of both systolic and diastolic dysfunction. In addition, left ventricular mass increased with pacing and remained elevated at 8 and 12 weeks of recovery. Four of these dogs studied at 6 months of recovery showed similar left ventricular abnormalities. CONCLUSION: Ten weeks of rapid ventricular pacing creates a long-term model of left ventricular dysfunction.

Animals↗
PubMed2000

Hepatitis C transmission and infection by orthotopic heart transplantation.

BACKGROUND: The transmission and clinical consequences of hepatitis C viral (HCV) infection acquired by orthotopic heart transplantation (OHT) from an HCV-infected donor to an HCV-naive recipient have not been well described. We report our experience in 5 HCV-naive patients who were transplanted with hearts from HCV-positive donors. All transplants occurred within a 1-year period. METHODS: After cardiac transplantation we retrospectively examined the recipients' clinical course, liver-associated enzymes, HCV-antibody serology, quantitative HCV RNA level, and HCV genotype. RESULTS: Five subjects with rapidly deteriorating heart failure and negative serum antibodies to HCV received an emergent OHT from a donor known to be infected with HCV. Liver-associated enzymes peaked at 2 to 6 weeks post-transplant: mean peak alanine aminotransferase was 180 U/L (normal, 9 to 52) and aspartate aminotransferase was 111 U/L (normal, 14 to 36). Liver enzymes had returned to normal limits by 6 and 12 months post-OHT. At a mean 15 months after transplantation, only 1 of 5 patients has developed antibodies to HCV, but 4 of 5 have evidence of infection, as shown by serum HCV RNA. No patient has developed evidence of liver failure. CONCLUSIONS: (1) Transmission of HCV from an HCV-positive donor to an HCV-naive recipient at the time of OHT is likely. (2) Antibodies to HCV post-OHT may remain negative for more than 1 year in these patients. (3) Hepatitis C viral RNA using polymerase chain reaction should be the test of choice for diagnosis of HCV infection post-OHT. (4) Hepatitis C viral donor hearts should be limited to critically ill patients in extremis until the long-term consequences of acquisition of HCV by an OHT recipient are known.

Aged↗
PubMed2000

Early post-transplant lymphoproliferative disease following heart transplantation in the absence of lymphocytolytic induction therapy.

We report a case of post-transplant lymphoproliferative disease presenting as a disseminated polymorphous B-cell lymphoma involving the cardiac allograft 3 months following transplantation in a recipient who did not receive anti-lymphocyte induction immunosuppression. In situ hybridization for the lytic Epstein-Barr virus marker NOT I was positive within a lymphocytic infiltrate on endomyocardial biopsy. Our case is the third of early post-transplant lymphoproliferative disease (within 6 months of transplantation) involving the heart allograft in the absence of anti-lymphocyte induction immunosuppression. Post-transplant lymphoproliferative disease of the heart allograft should be considered in the presence of an atypical cardiac lymphocytic infiltrate, with possible differentiation from allograft rejection using in situ hybridization for Epstein-Barr virus.

Drug Therapy, Combination↗
PubMed2000

Circulatory management of the unstable cardiac patient.

The objective of this article is to provide an orderly and concise approach to the treatment of the unstable cardiac surgery patient. The common causes of hemodynamic instability in this patient population are reviewed. The various pharmacologic, mechanical, and electric therapeutic options available for each clinical situation are explored, and a sequential treatment algorithm is developed.

Assisted Circulation↗
PubMed1999

Cardiovascular effects of inhaled nitric oxide in a canine model of cardiomyopathy.

BACKGROUND: The inhalation of nitric oxide (NO) in patients with heart failure decreases pulmonary vascular resistance (PVR) and is associated with an increase in pulmonary artery wedge pressure (PAWP). The mechanism for this effect remains unclear. METHODS: In dogs rapid-paced for 8 weeks to induce cardiac dysfunction, we performed left ventricular pressure-volume analysis of unpaced hearts in situ to determine whether during NO inhalation (80 ppm), the mechanism for the rise in PAWP is due to: 1) primary pulmonary vasodilation; 2) a direct negative inotropic effect; or 3) impairment of ventricular relaxation. RESULTS: Inhalation of NO decreased PVR by 51%+/-3.8% (257+/-25 vs 127+/-18 dynes x sec x cm(-5) [NO 80 ppm]; p < 0.001) and increased PAWP (15.4+/-2.4 vs 18.1+/-2.6 mm Hg [NO 80 ppm]; p < 0.001). Calculated systemic vascular resistance remained unchanged. Left ventricular (LV) end-diastolic pressure rose (16.4+/-1.9 vs 19.1+/-1.8 mm Hg [NO 80 ppm]; p < 0.001), as did LV end-diastolic volume (83.5+/-4.0 vs 77.0+/-3.4 mL [NO 80 ppm]; p = 0.006). LV peak +dP/dt was unchanged by NO (1,082+/-105 vs 1,142+/-111 mm Hg/sec [NO 80 ppm]; p = NS). There was a trend toward a stroke volume increase (17.4+/-1.2 vs 18.8+/-1.3 mL; p = NS), but the relaxation time constant and end-diastolic pressure-volume relation were both unchanged. CONCLUSIONS: In this canine model of cardiomyopathy, inhaled NO decreases pulmonary vascular resistance. The associated increase in left ventricular filling pressure appears to be secondary to a primary pulmonary vasodilator effect of NO without primary effects on the contractile or relaxation properties of the left ventricle.

Administration, Inhalation↗
PubMed1999

Management of exsanguinating hemoptysis during cardiopulmonary bypass.

BACKGROUND: Large-volume hemoptysis during cardiopulmonary bypass is an infrequent, but life-threatening event. Rapid airway clearance and control are the primary prerequisites for successful management. METHODS: The cases of 3 patients with different sources of exsanguinating hemoptysis during cardiopulmonary bypass managed initially with rigid bronchoscopy were reviewed. RESULTS: In all patients, airway control was rapidly established and weaning from cardiopulmonary bypass CPB was accomplished. Two patients survived the operative procedure. The other patient died in the operating room of unremitting bilateral pulmonary hemorrhage. CONCLUSIONS: Major hemoptysis during cardiopulmonary bypass is best dealt with initially by rapid airway control and cessation of bypass in an expeditious manner. An algorithm for suggested management is provided. The rigid bronchoscope is the optimal tool for initial management and it should always be available. Definitive treatment is determined by the cause and the persistence of hemorrhage once these maneuvers have been performed.

Aged↗
PubMed1999

Dynamic cardiomyoplasty: at the crossroads.

BACKGROUND: Dynamic cardiomyoplasty remains a promising, but still unproven surgical treatment for patients with end-stage heart failure. Lack of a clear survival advantage and ongoing misunderstanding of its mechanism of action have hindered its acceptance as a treatment alternative for patients with end-stage heart failure. This review seeks to update current clinical results and practice of dynamic cardiomyoplasty and to present its likely mechanism of action. METHODS: The method involved a literature review. RESULTS: More than 600 patients have undergone dynamic cardioplasty since 1985. Improvement in average New York Heart Association class was noted in 80% to 85% of hospital survivors. Operative mortality has decreased from 31% in Phase I to less than 3% in the ongoing Phase III trial. Clinical work as well as recent animal work supports the hypothesis that through a combination of long-term elastic constraint and active dynamic assist, dynamic cardiomyoplasty decreases myocardial wall stress associated with the remodeling process of progressive heart failure. CONCLUSIONS: Though dynamic cardiomyoplasty can be shown to limit the remodeling process of heart failure in animal studies and some patients, its ultimate role in the treatment of heart failure will depend on the outcome of randomized, controlled studies.

Cardiomyoplasty↗
PubMed1998

Long-term dynamic cardiomyoplasty improves chronic and acute myocardial energetics in a model of left ventricular dysfunction.

BACKGROUND: We present the first long-term evaluation of myocardial energetics after dynamic cardiomyoplasty (CMP) in a model of left ventricular (LV) dysfunction. METHODS AND RESULTS: Seventeen dogs underwent rapid ventricular pacing (RVP) to create heart failure. Eight dogs were randomly selected to undergo cardiomyoplasty. All dogs continued RVP for 6 additional weeks, whereas the CMP dogs underwent a simultaneously delivered synchronized muscle wrap conditioning protocol. After termination of RVP at 10 weeks in all dogs, myoplasty dogs continued to receive muscle wrap stimulation until the terminal study. Pressure-volume analysis to assess LV energetics was conducted at baseline and 4 weeks and 3 months after termination of RVP (6 months after baseline). At 6 months, CMP dogs displayed enhanced contractility, lower volumes, and more optimal energetics compared with control animals. Acute muscle wrap stimulation further increased effective contractility and myocardial efficiency compared with unassisted beats. CONCLUSIONS: The decrease in NYHA functional class that occurs in patients after dynamic cardiomyoplasty may be secondary to its beneficial effects on long-term myocardial function, volume, and energetics.

Animals↗
PubMed1998

Lipoprotein(a) levels and heart transplantation atherosclerosis.

BACKGROUND: Elevated serum lipoprotein(a) [Lp(a)] levels are associated with the development of native coronary atherosclerosis. The association between increased levels of Lp(a) and the development of accelerated cardiac allograft vasculopathy (ACAV) in patients who have undergone orthotopic heart transplantation has not been firmly established. METHODS AND RESULTS: We studied 74 consecutive heart transplant recipients with at least 1 year survival to determine the relation between Lp(a) and the presence of ACAV. Recipient and donor clinical and laboratory parameters, including mean serum Lp(a) levels, were obtained. ACAV was defined angiographically as > or =30% stenosis in one or more epicardial arteries. ACAV 1 year after heart transplantation was angiographically present in 26 (35%) patients. Mean donor age (36 +/- 13 years [ACAV (+)] vs 28 +/- 10 years, [ACAV (-)]; p = 0.004) and mean serum triglyceride levels 6 months after transplantation (286 +/- 275 mg/dl [ACAV (+)] vs 169 +/- 85 mg/dl [ACAV (-)]; p = 0.025) were univariate predictors of ACAV. No significant difference in mean serum Lp(a) levels was observed (20 +/- 19 mg/dl [ACAV (+)] vs 30 +/- 30 mg/dl [ACAV (-)]; p = NS). Donor age was the single greatest independent predictor of ACAV by multivariate logistic regression (p = 0.02). CONCLUSIONS: Lp(a) does not appear to be a risk factor for the development of ACAV 1 year after heart transplantation. Further studies are needed to define the influence of serum Lp(a) on the development of cardiovascular disease after orthotopic heart transplantation.

Adult↗
PubMed1998

Management of sternal and abdominal wounds in a pediatric heart transplant patient.

A 14-year-old girl with congenital heart disease underwent ventricular assist device placement before cardiac transplantation. The inability to close her abdominal fascia necessitated the placement of Prolene mesh, which subsequently became exposed and contaminated when her incision dehisced. Stable closure was obtained with Vicryl mesh and a rectus abdominis turnover flap. Her posttransplant course was notable for compression of the donor heart, necessitating prolonged open sternotomy. She failed an attempt at delayed sternal closure due to compression of the right ventricle by the sternum. In addition to standard pectoralis advancement flaps, a pedicled osseous sternal flap based on her left internal mammary artery was developed to avoid ventricular compression yet still provide some protection to the mediastinum. Alternative uses of this vascularized bone flap to assist with chest wall reconstruction are discussed.

Abdomen↗
PubMed1997

Stabilization of chronic remodeling by asynchronous cardiomyoplasty in dilated cardiomyopathy: effects of a conditioned muscle wrap.

BACKGROUND: Dynamic cardiomyoplasty is a promising new therapy for dilated cardiomyopathy. The girdling effects of a conditioned muscle wrap alone have recently been postulated to partly explain its mechanism. We investigated this effect in a canine model of chronic dilated cardiomyopathy. METHODS AND RESULTS: Twenty dogs underwent rapid ventricular pacing (RVP) for 4 weeks to create a model of dilated cardiomyopathy. Seven dogs were then randomly selected to undergo subsequent cardiomyoplasty, and all dogs had 6 weeks of additional RVP. The cardiomyoplasty group also received 6 weeks of concurrent skeletal muscle stimulation consisting of single twitches delivered asynchronously at 2 Hz to transform the wrap without active assistance. All dogs were studied by pressure-volume analysis and echocardiography at baseline and after 4 and 10 weeks of pacing. Systolic indices, including ejection fraction (EF), end-systolic elastance (Ees), and preload-recruitable stroke work (PRSW) were all increased at 10 weeks in the wrap versus controls (EF, 34.0 versus 27.1, P=.008; Ees, 1.65 versus 1.26, P=.09; PRSW, 35.9 versus 25.5, P=.001). Ventricular volumes, diastolic relaxation, and left ventricular end-diastolic pressures stabilized in the cardiomyoplasty group but continued to deteriorate in controls. Both the end-systolic and end-diastolic pressure-volume relationships shifted farther rightward in controls but remained stable in the cardiomyoplasty group. CONCLUSIONS: In addition to potential benefits from active systolic assistance, benefits from dynamic cardiomyoplasty appear to be partially accounted for by the presence of a conditioned muscle wrap alone. This conditioned wrap stabilizes the remodeling process of heart failure, arresting progressive deterioration of systolic and diastolic function.

Animals↗