First World Report of Internal Power Cable Repair in Left Ventricular Assist Device Jarvik 2000: Case Report.

BACKGROUND: There are limited clinical reports concerning internal power cable fixing in left ventricular assist device (L-VAD) patients. Actually there are no reports in the literature about Jarvik 2000 internal cable repair. We show the first description of a technique for surgical reparation of such a fatal complication. PATIENT HISTORY: The patient was a 62-year-old woman who had L-VAD implantation (Jarvik 2000) with outflow graft apposition in descending thoracic aorta through left thoracotomy access, in 2009. She arrived urgently on January 25, 2014 for Jarvik 2000 dysfunction correlated with head movements. The neck X-rays revealed the rupture of one of the nine power cables located inside the neck and the damaging of two more cables nearby to be ruptured. On the same day she got pump failure due to the final interruption of the remaining two cables, we were obliged to install femoro-femoral extracorporeal membrane oxygenation (ECMO) assistance, to repair the power cables, approaching them through a pacemaker extension cable. The L-VAD outflow was occluded with vascular ball occluder inserted via right axillary artery under fluoroscopy before ECMO installation. At the end the ECMO assistance was interrupted and the Jarvik 2000 was turned back on. The patient was dismissed from the hospital 12 days after the procedure. DISCUSSION: At the moment the international literature is poor regarding this issue. This case provides evidence that in emergency conditions ECMO assistance is mandatory and a hybrid surgical and radiological approach could help to repair the damage in safe conditions.

Longitudinal Strain Stress-Echo Evaluation of Aged Marginal Donor Hearts: Feasibility in the Adonhers Project.

BACKGROUND: The Adonhers (aged donor heart rescue by stress-echo protocol) Project was created to resolve the current shortage of donor hearts. One of the great limits of stress echo is the operator dependency. Speckle-tracking echocardiography (STE), offering a quantitative objective analysis of myocardial deformation, may help to overcome this limit. This study aimed to verify feasibility of a stress-strain echo analysis in selection of aged donor hearts for heart transplant. METHODS: From February 2014 to October 2015, 22 marginal candidate donors (16 men) ages 58 ± 4 years were initially enrolled. After legal declaration of brain death, all marginal donors underwent bedside echocardiography, with baseline and (when resting echocardiography was normal) dipyridamole (0.84 mg/kg in 6 minutes) stress echo. In all patients, left ventricular (LV) longitudinal myocardial deformation was obtained by STE in the 4-, 2-, and 3-chamber views, obtaining the average global longitudinal strain (GLS). GLS was assessed at baseline and at the peak of stress echo. RESULTS: Baseline echocardiography showed wall motion abnormalities in 9 patients (excluded from donation). Stress echocardiography was performed in the remaining 13 patients. Results were normal in 8, who were uneventfully transplanted in marginal recipients. Stress results were abnormal in 5 (excluded from donation). STE was obtained in all cases (100% feasibility) and ΔGLS was significantly different between normal and pathological stress-echo (+13.2 ± 5.2 versus -6.1% ± 3.1%, P = .0001, respectively). CONCLUSIONS: STE showed an excellent feasibility in analysis of LV myocardial longitudinal strain at baseline and at the peak of stress echo of marginal heart donors. Further experience is needed to confirm STE as a valuable additional mean to better interpret stress echo in marginal donors.

C2 and C0 values for monitoring cyclosporine therapy in stable heart transplant recipients.

INTRODUCTION: We sought to evaluate the behavior of C2 values and their correlation with acute rejection episodes and cyclosporine (CyA) side effects in heart transplant patients whose immunosuppressive therapy, was monitored with C0 trough levels. METHODS: Sixty stable patients who had received heart transplants from 3 months to 60 months prior were randomly observed from September 2001 to June 2004. Four area under the concentration-time curves (AUC) were performed on each patient, a total of 240 AUC curves. RESULTS: Regarding the variability of CyA absorption, two groups of patients were distinguished: group A, "constant absorbers," namely, low variability (<15%) of CyA absorption; group B, "inconstant absorbers" patients with higher (>15%) variability of absorption. Group B patients showed more acute rejection episodes (41%) than group A (19%). CyA side effects were more serious in patients with higher variability of absorption: systemic hypertension, neurological disorders, hyperlipidemia, and gum hyperplasia; Group B patients who developed CyA side effects showed higher maximum and mean C2 levels (P < .05) than group A patients. No differences were found with regard to renal dysfunction between the two groups: all patients showed a mean increase of serum creatinine by at least 50% compared to the baseline value. CONCLUSION: Higher C2 levels were not sufficient to predict acute rejection compared to lower but constants, C2 levels. Patients with inconstant absorption were more often overexposed to CyA than underexposed, developing more side effects than patients with lower variability of absorption. Monitoring CyA therapy with C0 and C2 may prevent over- or underexposure to the drug.

Risk factors for smoking abuse after heart transplantation.

Patients (n = 103) were studied before heart transplantation with regard to smoking habits by means of a clinical interview, and 81 were submitted to Minnesota Multiphasic Personality Inventory (MMPI). After a mean time of 50.8 +/- 24.2 months from transplant, they were once again interviewed to ascertain their smoking habits after intervention. Nonsmokers (35 of 103) were still nonabusers. Of the remaining 68 patients who ceased smoking before heart transplant, 12 (17.6%) had returned to tobacco abuse. Dividing these 68 patients into two groups based upon the length of smoking cessation before heart transplant (less than 1 year: short term [ST] more than 1 year: long term [LT]), we noticed that the ST group showed a much greater rate of reabuse (8 of 20, 40%) than the LT group (4 of 48, 8.3%, P =.006). Analyzing six scales of MMPI, we found a statistically different score for self-control ability (scale K) in ST and LT smokers compared to nonsmokers (45.5 and 45.5 vs 51.2, P =.026), and for difficult adaptation (scale Ma) in ST compared both to LT smokers and nonsmokers (ST 57, LT 50.5, NS 47.6; P =.042 LT vs ST, P =.0005 ST vs NS). We concluded that patients who have recently decided to stop smoking and show after MMPI compilation a score of >50 for K and <50 for Ma scale have a higher risk of reabuse and need a greater effort by the transplant team to reinforce their will to stop smoking.

Right pneumonectomy for adenocarcinoma stage IIIA-N2 in a heart transplant patient after induction chemotherapy.

Lung tumors are the most frequent solid tumor in the heart transplant population. Unfortunately, most of these patients are in an advanced stage of disease at the time of presentation, which carries a poor prognosis. We present a heart transplant patient with histologically proven. Stage IIIA-N2 bronchogenic adenocarcinoma who had complete lymph-node downstaging after induction chemotherapy and underwent a complete tumor resection by right pneumonectomy.

Smooth muscle cells of the media in the dilatative pathology of ascending thoracic aorta: morphology, immunoreactivity for osteopontin, matrix metalloproteinases, and their inhibitors.

The etiopathogenesis of thoracic aortic aneurysms is currently an issue of debate. The present study investigated ultrastructural, morphometric, and immunohistochemical aspects of smooth muscle cells (SMCs) in chronic aneurysm of the thoracic aorta (aneurysm group), aortic dilatation associated with valvular disease (valvular group), and dissection of the thoracic aorta (dissection group). Fragments of the ascending aorta that had been taken from the patients during coronary bypass surgery were used as controls. No significant difference was observed in the density of SMCs between the 3 pathologic groups put together and the controls. Only separate analysis of SMC density in each of the pathologic groups showed that the valvular group samples had significantly smaller amounts of SMCs in the internal layer of the media than the dissection group samples and controls. Ultrastructural analysis, in situ end labeling, propidium iodide assay, and DNA laddering did not show apoptosis of SMCs in the samples investigated. Ultrastructure of SMCs characteristic of the synthetic phenotype, together with increased expression of osteopontin in the media of pathologic thoracic aortas indicated the transition of SMCs from the contractile to the synthetic phenotype. Immunohistochemical investigation showed that medial SMCs in the samples taken from aortas of all 3 pathologic groups expressed stronger immunoreactivity for matrix metalloproteinase 1, 2, and 9 and tissue inhibitor of metalloproteinase 1 and 2 than the controls. The present study shows that during the formation of aneurysms, dissection of the thoracic aorta, or aortic dilatation associated with valvular disease, loss of SMCs was not of great importance with respect to their transition from the contractile to the synthetic type in leading to increased production of matrix metalloproteinases.

Operation for acute type A aortic dissection in octogenarians: is it justified?

BACKGROUND: With the progressive aging of Western populations, cardiac surgeons are faced with treating an increasing number of elderly patients. Controversy exists as to whether the expenditure of health care resources on the growing elderly populations represents a cost-effective approach to resource management. The potential to avoid surgery in patients with little chance of survival and poor quality of life would spare unnecessary suffering, reduce operative mortality, and enhance the use of scarce resources. METHODS: We reviewed the records of 24 consecutive patients aged 80 years or older (mean age 83 years, range 80-93 years) who underwent operations for acute type A dissection from 1985 through 1999. No patient with acute type A dissection was refused surgery because of age or concomitant disease. Seventeen patients were men. Preoperatively, none of the patients was moribund, although 66% had hemodynamic instability and 41% experienced cerebral ischemia. All patients had one or more associated pathologic conditions. Hospital mortality and morbidity models, based on our overall experience with 197 patients operated on for acute type A aortic dissection during the period of the study, were developed by means of multivariate logistic regression with preoperative and intraoperative variables used as independent predictors of outcome. RESULTS: Overall hospital mortality was 83%. Intraoperative mortality was 33%. All patients who survived the operation had one or more postoperative complications. Mean hospital stay was 37 days with a total of 314 days in the intensive care unit (average 19 days, median 17 days). None of the survivors (4 patients) discharged from the hospital was able to function independently and their survival at 6 months was 0%. Statistical analysis of the overall experience with operations for type A acute aortic dissection confirmed that age in excess of 80 years is the most important independent patient risk factor associated with 30-day mortality and morbidity. CONCLUSIONS: Operations for acute type A dissection performed on octogenarians involve increased hospital mortality and morbidity. Short-term survival is unfavorable and is associated with a poor quality of life. Without additional corroborative studies to endorse the present findings, the use of age as a parameter to limit access of patients to expensive medical resources remains an unsubstantiated concept. In the context of acute type A aortic dissection, however, the hypothesis that older patients should be denied such a complicated surgical intervention to conserve resources is supported by the presented data.

The properties of the pacemaker current I(F)in human ventricular myocytes are modulated by cardiac disease.

The pacemaker current I(f)is present in ventricular myocytes from the human failing heart where it may contribute to arrhythmogenesis. The role of cardiac disease in the modulation of I(f)expression is still uncertain. We studied the functional expression and properties of I(f)in human ventricular myocytes isolated from control donor hearts or from explanted failing hearts of patients with ischemic and dilated cardiomyopathy. In patch-clamped cells, I(f)was elicited by hyperpolarization. Membrane capacitance (C(m)) was significantly higher in dilated cardiomyopathy than in control or ischemic cardiomyopathy. I(f)was present in all ischemic and dilated cardiomyopathy tested cells and in 76% of control cells. In ischemic and dilated cardiomyopathy, I(f)amplitude measured at -120 mV was significantly greater than in control. However, I(f)density (i.e. current normalized to C(m)) was significantly higher in ischemic cardiomyopathy (2.0+/-0.2 pA/pF) than in dilated cardiomyopathy (1.2+/-0.1 pA/pF) or control (1.0+/-0.1 pA/pF). In diseased hearts, the activation curve was significantly shifted to more positive values compared to control. The slope of the fully-activated I-V relations was greater in ischemic cardiomyopathy than in dilated cardiomyopathy or control (P<0.05) while the intercept with the x -axis (V(rev)) was similar. In conclusion, I(f)is overexpressed in human ventricular myocytes from failing hearts; its functional expression seems related to the etiology of the disease, being higher in ischemic than in dilated cardiomyopathy, and not to the degree of cell hypertrophy.

Electrophysiologic effects of lercanidipine on repolarizing potassium currents.

Blockade of cardiac repolarizing potassium channels by drugs may result in QT-interval prolongation, eventually degenerating into "torsades de pointes," a life-threatening arrhythmia. Lercanidipine (LER) is a recently introduced lipophilic calcium antagonist with no cardiodepressant activity and long-lasting antihypertensive action. Its chemical structure is characterized by the presence of a diphenylpropylaminoalkyl group, which is present in some of the drugs that have been reported to cause QT-interval prolongation. Our previous data demonstrated that LER blocks L-type calcium channels without affecting sodium current; however, no data are available concerning its effects on cardiac potassium channels. Transient outward (I(to)), delayed rectifier (I(K)), background currents, and action potential (AP) profile were measured from patch-clamped ventricular myocytes isolated from rat, guinea pig, or human hearts using enzymatic dissociation procedures. LER did not affect I(K) (and I(Kr)) density and activation curve in guinea pig myocytes; the reversal potential of the background current (I(K1)) and its slope were not changed by the drug. Maximal diastolic potential (MDP) and duration of the AP measured at -60 mV (APD(-60)) were not significantly changed. I(to) density and activation curves measured in rat myocytes were similar in the absence and presence of 1 or 10 microM LER. Finally, the effect of LER was tested in human ventricular myocytes: superfusion with 1 microM LER did not affect MDP and APD(-60). I(to) density and the midpoint of activation and inactivation curves were similar in the absence and presence of LER. In conclusion, our data demonstrate that LER does not affect repolarizing potassium currents and action potential profile recorded from guinea pig, rat, and human ventricular myocytes. It is unlikely that LER could cause QT prolongation in vivo.

Localized dissection and delayed rupture of the abdominal aorta after extracorporeal shock wave lithotripsy.

Extracorporeal shock wave lithotripsy (ESWL) represents the preferred treatment for most upper ureteric and renal calculi. Complication rates associated with ESWL are low, justifying the enthusiasm and acceptance of this treatment modality. As the technique has become more widely available, some deleterious effects on the kidneys and the surrounding tissues are increasingly recognized. We report on the rupture of a severely calcified abdominal aorta in a 65-year-old man who underwent 3 months of ESWL treatment earlier for renal calculi. The patient was seen with an acute recrudescence of a long-standing abdominal and left flank pain, which began immediately after the last of the three sessions of ESWL and was associated with an episode of hypotension that occurred an hour before admission. Patient history and chronologic course of events strongly suggest the role of ESWL in the genesis of abdominal aorta rupture.

Evolution toward dissection of an intramural hematoma of the ascending aorta.

Intramural hematoma of the aorta is a condition increasingly observed in clinical practice. Uncertainty exists whether such lesions represent a different pathology or simply the precursors of classic dissecting aneurysm. The patient was a 76-year-old woman with intramural hematoma of the ascending aorta. Clinical course, progression of the lesion to type A aortic dissection, and surgical treatment are described. Although natural history of intramural hematoma of the ascending aorta is not clearly elucidated, the case presented confirms that the evolution toward intimal flap formation is possible and that we cannot foresee the stabilization of these lesions. We stress that intramural hematoma of the ascending aorta has to be managed as an aortic type A dissection and that aggressive treatment is advisable.

Axillary artery cannulation in type a aortic dissection operations.

BACKGROUND: Femoral arteries are the preferred site of peripheral cannulation for arterial inflow in type A aortic dissection operations. The presence of aortoiliac aneurysms, severe peripheral occlusive disease, atherosclerosis of the femoral vessels, and distal extension of the aortic dissection may preclude their utilization. Axillary artery cannulation may represent a valid alternative in these circumstances. METHODS: Between January 15, 1989, and August 20, 1998, in our institution, 22 of 152 operations (14.4%) for acute type A aortic dissection were performed with the use of the axillary artery for the arterial inflow. Axillary artery cannulation was undertaken in the presence of femoral arteries bilaterally compromised by dissection in 12 patients (54.5%), abdominal aorta and peripheral aneurysm in 5 patients (22.7%), severe atherosclerosis of both femoral arteries in 3 patients (13. 6%), and aortoiliac occlusive disease in 2 patients (9.1%). In all patients, distal anastomosis was performed with an open technique after deep hypothermic circulatory arrest. Retrograde cerebral perfusion was used in 9 patients (40.9%). RESULTS: Axillary artery cannulation was successful in all patients. The left axillary artery was cannulated in 20 patients (90.9%), and the right axillary artery was cannulated in 2 patients (9.1%). Axillary artery cannulation followed an attempt of femoral artery cannulation in 15 patients (68. 2%). All patients survived the operation, and no patient had a cerebrovascular accident. No axillary artery thrombosis, no brachial plexus injury, and no intraoperative malperfusion were recorded in this series. Two patients (9.1%) died in the hospital of complications not related to axillary artery cannulation. CONCLUSIONS: In patients with type A aortic dissection in whom femoral arteries are acutely or chronically diseased, axillary artery cannulation represents a safe and effective means of providing arterial inflow during cardiopulmonary bypass.