Pectoral muscle mass is not a robust prognostic factor for survival after left ventricular assist device (LVAD) implantation.

BACKGROUND: Left ventricular assist devices (LVAD) are an established treatment for end-stage left ventricular heart failure. Parameters are needed to identify the most appropriate patients for LVADs. This study aimed to evaluate pectoral muscle mass and density as prognostic parameters. METHODS: This single-center study included all patients with LVAD implantation between January 2010 and October 2017 and a preoperative chest CT scan. Pectoral muscle mass was assessed using the Pectoralis Muscle Index (PMI, surface area indexed to height, cm2/m2) and pectoral muscle density by Hounsfield Units (HU). Overall mortality was analyzed with Kaplan-Meier survival analysis and 1-year and 3-year mortality with receiver operating characteristic (ROC) curves and Cox regression models. RESULTS: 57 patients (89.5% male, mean age 57.8 years) were included. 64.9% of patients had end-stage left ventricular failure due to ischemic heart disease and 35.1% due to dilated cardiomyopathy. 49.2% of patients had preoperative INTERMACS profile of 1 or 2 and 33.3% received mechanical circulatory support prior to LVAD implantation. Total mean PMI was 4.7 cm2/m2 (± 1.6), overall HU of the major pectoral muscle was 39.0 (± 14.9) and of the minor pectoral muscle 37.1 (± 16.6). Mean follow-up was 2.8 years (± 0.2). Mortality rates were 37.5% at 1 year and 48.0% at 3 years. Neither PMI nor HU were significantly associated with overall mortality at 1-year or 3-year. CONCLUSIONS: The results of our study do not confirm the association between higher pectoral muscle mass and better survival after LVAD implantation previously described in the literature.

Impact of psoas muscle evaluation on clinical outcomes in patients undergoing left ventricular assist device implantation.

AIMS: The measurement of muscle mass reflects the physical components of frailty, which might affect postoperative outcomes in patients undergoing left ventricular assist device (LVAD) implantation. The aim of this study was to investigate the relationship between preoperative skeletal muscle evaluation and clinical outcomes in patients undergoing LVAD implantation. METHODS: From January 2010 to December 2017, a total of 63 patients were enrolled in this single-centre study. A retrospective analysis of preoperative abdominal computed tomography (CT) for psoas muscle index (PSMI) and Hounsfield-Units of the Psoas Muscle (PSHU) at the level of the mid-L4 vertebra was performed. RESULTS: Sixty-three patients (male; n = 49, 78%), with a mean age of 58.0 ±â€Š11.8 years, were treated with LVAD due to dilated (32%) or ischemic cardiomyopathy (68%). Among them, 43 patients (68.3%) were categorized in the Interagency Registry for Mechanically Assisted Circulatory Support profile I. The survival rate was 73.0% at 30 days and 44.4% at 1 year. Receiver-operating characteristic (ROC) curve analyses revealed that PSMI was a significant numeric predictor of 1-year mortality (P = 0.04). In contrast, PSHU displayed a significant predictive potential for pericardial effusion (P = 0.03) and respiratory insufficiency (P = 0.01). In addition, comparative ROC curve analysis revealed no significant difference in the predictive potential of PSMI and PSHU. CONCLUSION: Preoperative PSMI might be a predictor of 1-year mortality in patients undergoing LVAD implantation. In contrast, the PSHU seemed to potentially assume postoperative adverse events in this study. Thus, the evaluation of the preoperative psoas muscle using CT appears to be promising.

Risk and Consequences of Postoperative Delirium in Cardiac Surgery.

BACKGROUND: Delirium is a common complication after cardiac surgery that leads to increased costs and worse outcomes. This retrospective study evaluated the potential risk factors and postoperative impact of delirium on cardiac surgery patients. METHODS: One thousand two hundred six patients who underwent open-heart surgery within a single year were included. Uni- and multivariate analyses of a variety of pre, intra-, and postoperative parameters were performed according to differences between the delirium (D) and nondelirium (ND) groups. RESULTS: The incidence of delirium was 11.6% (n = 140). The onset of delirium occurred at 3.35 ± 4.05 postoperative days with a duration of 5.97 ± 5.36 days. There were two important risk factors for postoperative delirium: higher age (D vs. ND, 73.1 ± 9.04 years vs. 69.0 ± 11.1 years, p < 0.001) and longer aortic cross-clamp time (D vs. ND, 69.8 ± 49.9 minutes vs. 61.6 ± 53.8 minutes, p < 0.05). We found that delirious patients developed significantly more frequent postoperative complications, such as myocardial infarction (MI) (D vs. ND, 1.43% [n = 3] vs. 0.28% [n = 2], p = 0.05), cerebrovascular accident (D vs. ND, 10.7% [n = 15] vs. 3.75% [n = 40], p < 0.001), respiratory complications (D vs. ND, 16.4% [n = 23] vs. 5.72% [n = 61], p < 0.001), and infections (D vs. ND, 36.4% [n = 51] vs. 16.0% [n = 170], p < 0.001). The hospital stay was longer in cases of postoperative delirium (D vs. ND, 23.2 ± 13.6 days vs. 17.4 ± 12.8 days, p < 0.001), and fewer patients were discharged home (D vs. ND, 56.0% [n = 65] vs. 66.8% [n = 571], p < 0.001). CONCLUSIONS: Because the propensity for delirium-related complications is high after cardiac surgery, a practical, preventative strategy should be developed for patients with perioperative risk factors, including higher age and a longer cross-clamp time.

Conversion of Atrial Fibrillation after Cardiosurgical Procedures by Vernakalant® as an Atrial Repolarization Delaying Agent (ARDA).

BACKGROUND: Postoperative, new-onset atrial fibrillation (POAF) is one of the most common complications after cardiosurgical procedures. Vernakalant has been reported to be effective in the conversion of POAF. The aim of this study was to evaluate the efficacy and safety of vernakalant for atrial fibrillation after cardiac operations, and to investigate predictors for the success of vernakalant treatment. Patients and Methods: Post-cardiac surgery patients with new-onset of atrial fibrillation (AF) were consecutively enrolled in this study. Demographic data as well as intraoperative and postoperative parameters were analyzed. Vernakalant administration was primarily started 5.5 hours after new-onset POAF: 3 mg/kg intravenously over 10 min, and in case of non-conversion, a second dose of 2 mg/kg intravenously over 10 min. Results: 129 consecutive patients (70.2 ± 9.1 years) were included: 61 patients with coronary artery bypass graft (CABG) surgery, 49 patients with isolated valve procedures, and 19 patients with combined procedures (CABG and valve). Conversion in sinus rhythm was achieved after the first vernakalant dose in 57 patients (44%), and after the second dose in 41 patients (32%). The mean time to conversion was 13.7 ± 14.1 min. The patients receiving valve procedures depicted a significantly lower conversion rate. The following variables lowered conversion rate: no preoperative beta blocker, postoperative troponin levels >500 ng/L, and systolic blood pressure >140 mmHg. At the first follow-up, 92% of the converted patients showed sinus rhythm, while 80% of the non-responders showed sinus rhythm (P < .01). Conclusions: The POAF was effectively converted by vernakalant. The conversion rate of POAF after valve surgery was lower when compared to isolated CABG.

Anxiety and Depression in Patients Undergoing Mitral Valve Surgery: A Prospective Clinical Study.

BACKGROUND: Impending cardiac surgery presents an existential experience that may induce psychological trauma. Moreover, quality of life long after successful coronary artery bypass graft surgery (CABG) can be impaired. AIM: The aim of this study was to describe the time course of anxiety and depression in patients undergoing mitral valve surgery and compare it with our earlier results of patients undergoing CABG, a disease that is likely to be related to psychosomatic disorders. We hypothesized that patients undergoing mitral valve surgery can better manage stresses of cardiac surgery than patients undergoing CABG. PATIENTS AND METHODS: Of 117 patients undergoing mitral valve surgery, 100 patients (22 to 87 years; 53 females) completed the study and were interviewed before (pre), 1 week after (early), and 6 months after (late) surgery. The Hospital Anxiety and Depression Scale (HADS) was employed. RESULTS: The proportion of patients with elevated anxiety scores (AS ≥ 8) was higher than normal (19.8%): pre, 33.0%; early, 28.0%; and was normalized late (18.0%). Similarly, depression scores (DS ≥ 8) were increased: pre, 15.0%; early, 20.0%; and late 14.0%, respectively (normal: 3.2%). CONCLUSION: Coronary heart disease of CABG patients is presented as a systemic disorder, associated with both higher and postoperatively increased distress levels than in mitral valve patients. Anxiety and depression should be recognized as possible symptoms of psychosomatic disorders necessitating psychotherapeutic intervention to prevent postoperative depression and warrant patient-perceived surgical outcome that is additionally affected by expectations with respect to treatment and individual coping capacities. HADS is recommended to screen for vulnerable patients in the clinical routine, and psychosomatic support should be provided.

A case of lethal spontaneous massive hemothorax in a patient with neurofibromatosis 1.

Neurofibromatosis type 1 is an autosomal dominant disease characterized by multiple dermatological disorders amongst others. Among the less frequent manifestations are vascular abnormalities. Here, we present a case of spontaneous massive hemothorax in a 39-year-old Caucasian woman with neurofibromatosis 1 and a thoracic meningocele with a lethal outcome despite extensive surgical intervention as well as intensive care measures. Spontaneous hemothorax is a rare, but potentially lethal complication of neurofibromatosis type 1, which necessitates quick and decisive intervention; endovascular embolization where possible, otherwise aggressive surgical intervention in unstable patients.

Cardiac stunning in the clinic: the full picture.

Cardiac stunning refers to different dysfunctional levels occurring after an episode of acute ischemia, despite blood flow is near normal or normal. The phenomenon was initially identified in animal models, where it has been very well characterized. After being established in the experimental setting, it remained unclear, whether a similar syndrome occurs in humans. In addition, it remained controversial, whether stunning was of any clinical relevance as it is spontaneously reversible. Hence, many studies continue to focus on the properties and mechanisms of stunning, although therapies seem more relevant for attenuating and treating myocardial ischemia/reperfusion (I/R) injury, i.e. to bridge until recovery. This article reviews the different facets of cardiac stunning, i.e. myocardial, vascular/microvascular/endothelial, metabolic, neural/neuronal, and electrical stunning. This review also displays where these facets exist and which clinical relevance they might have. Particular attention is directed to the different therapeutic interventions that the various facets of this I/R-induced cardiac injury might require. A final outlook considers possible alternatives to further reduce the detrimental consequences of brief episodes of ischemia and reperfusion.

Ca2+ sensitizer superior to catecholamine during myocardial stunning?

BACKGROUND: After open-chest cardiac surgery, ventricular function remains depressed (myocardial stunning). Catecholamines (epinephrine) improve ventricular function by increasing the intracellular Ca(2+) concentration. In parallel, the oxygen consumption is increased, so that the hitherto intact myocardium can be jeopardized. In the very insufficient ventricle, epinephrine can even become ineffective. Since Ca(2+) sensitizers provide another therapeutic avenue, the effects of epinephrine and levosimendan on postischemic hemodynamics were investigated. METHODS: After hemodynamic steady state, isolated, blood (erythrocyte-enriched Krebs-Henseleit solution)-perfused rabbit hearts were subjected to 25 min normothermic, no-flow ischemia and 20 min reperfusion. Heart rate (HR), cardiac output (CO), left ventricular pressure (LVP), coronary blood flow (CBF), and arterio-venous oxygen difference (AVDO(2)) were recorded during reperfusion and after administration of either epinephrine (n=16; 0.03 micromol), or levosimendan (n=11; 0.75 micromol) or epinephrine plus levosimendan (n=5). RESULTS: Epinephrine increased HR (19%, p=0.01) and improved hemodynamics in terms of CO (62%, p=0.0006), stroke volume SV (46%, p=0.02), stroke work W (158%, p=0.01), LVP(max) (58%, p=0.0001), maximal pressure increase dP/dt(max)(140%, p=0.0004), minimal pressure increase dP/dt(min) (104%, p=0.0002), LVP(ed) (-26%, p=0.02), and increased coronary resistance CR (31%, p=0.05). Epinephrine impaired hemodynamics in terms of AVDO(2) (+63%, p=0.003), myocardial oxygen consumption MVO(2) (+67%, p=0.0003) and MVO(2)/beat (+36%, p=0.01). External efficiency eta was increased by 92% (p=0.02). Levosimendan in postischemic hearts increased HR (32%, p=0.009) and improved hemodynamics in terms of CO (85%, p=0.01), SV (44%, p=0.03), W (115%, p=0.04), LVP(max) (95%, p=0.04), dP/dt(max) (133%, p=0.009), dP/dt(min) (121%, p=0.007), LVP(ed) (-63%, p=0.0006), and CR (-17%; n.s., p=0.1). It altered hemodynamics in terms of AVDO(2) (+7.0%; n.s., p=0.3) and MVO(2) (+32%, p=0.007) and MVO(2)/beat (+2.3%; n.s., p=0.4). External efficiency was increased by 307% (p=0.04). In five additional extremely dysfunctional rabbit hearts, epinephrine was ineffective. Additional levosimendan increased hemodynamics in terms of HR (56%; n.s., p=0.1), CO (159%, p=0.04), SV (89%, p=0.03), W (588%, p=0.02), LVP(max) (168%, p=0.03), dP/dt(max) (102%, p=0.005), dP/dt(min) (78%, p=0.006), LVP(ed) (-98%, p=0.0006), and CR (-50%, p=0.02). It altered hemodynamics in terms of AVDO(2) (-11%; n.s., p=0.05), MVO(2) (+131%, p=0.04) and MVO(2)/beat (+171%, p=0.03). External efficiency was increased by 212% (p=0.04). CONCLUSION: In contrast to epinephrine, levosimendan improves ventricular function without increasing oxygen demand, thereby considerably improving external efficiency. Even during epinephrine resistance in extremely dysfunctional hearts, levosimendan successfully improves ventricular function.

Evidence for palliative enlargement of the right ventricular outflow tract in severe tetralogy of Fallot.

OBJECTIVE: If the pulmonary artery (PA) tree in patients with Fallot's tetralogy (TOF) is extremely hypoplastic, a shunt procedure may be difficult and not desirable because of side-effects. Moreover, the failing catch-up growth of the pulmonary annulus is well known. In patients with a severe form of TOF, we performed palliative transannular patching of the right ventricular outflow tract. The early and long-term follow-up was evaluated. METHODS: Eleven patients (93 days (10-245 days); 3.5+/-0.7 kg (2.5-4.3 kg)) had highly symptomatic TOF (Hb: 18+/-2g/dl, SO2: 68+/-11%); angiographic diameters: RPA: 4.1 mm (2.5-6.4 mm), LPA: 3.4 mm (1.6-7.0 mm), PA trunc: 4.4 mm (2.5-7.0 mm). All 11 underwent transannular enlargement of the right ventricular outflow tract without closure of the ventricular septum defect. A PA index (cross-sectional area of the pulmonary arteries to BSA) was used to compare pre- and postoperative data. For follow-up, the patients were repetitively examined clinically and echocardiographically. RESULTS: Preoperative PA index was 87+/-40 mm2/m2 (normal: 330+/-35 mm2/m2). Postpalliation angiograms (age: 10-14 months) demonstrated a significant catch-up growth in nine patients (PA index from 99+/-40 to 310+/-54 mm2/m2) and inadequate growth in two patients (PA index 63 and 115 mm2/m2). Perioperative mortality was zero. Ten patients (43 months; 6-105 months) underwent elective repair. Six patients received pulmonary homograft valves (6-15 years after repair) because of severe pulmonary valve insufficiency and severe RV dilation. COMPLICATIONS: One patient died 10 months postpalliation due to pneumonia, one patient received a pacemaker after repair and died (2 months post-repair) due to pacemaker failure, a 5-year-old patient died 1 month after repair due to sepsis. All eight long-term survivors (12-17 years) are in excellent clinical condition. Echocardiography revealed good RV function and near normal diameters at peak systolic pressures between 25 and 50 mmHg. Only one patient developed brady-arrhythmia; a pacemaker was implanted 8 years after repair and 2 years after homograft implantation. CONCLUSIONS: In a very severe form of TOF, palliative right ventricular outflow tract construction may provide the potential for complete repair. In the presented high-risk patient group, mortality was not related to the hypoplastic pulmonary arteries. Obviously, all patients need pulmonary valve implantation in the long run.

Coronary flow reserve in hypertrophic obstructive cardiomyopathy assessed by intracoronary Doppler catheter.

BACKGROUND: In spite of progress in diagnosis and treatment, hypertrophic obstructive cardiomyopathy (HOCM) remains a serious medical problem. Among many issues, the pathophysiology of the coronary circulation in HOCM has not yet been fully examined. AIM: To assess coronary flow reserve in HOCM. METHODS: The study group consisted of 15 patients (6 males, 9 females, mean age 51+/-15 years) with typical echocardiographic signs of HOCM and without stenosis of the coronary arteries. Using an intracoronary Doppler catheter, the average peak velocity and the absolute coronary flow reserve were determined in the proximal, medial and distal parts of the left anterior descending (LAD) and the circumflex coronary artery (Cx) following administration of papaverine, substance P, and during pacing. The coronary square plane was calculated angiographically after substance P injection. The retrograde coronary flow and the relationship between the increase of the coronary square plane and the coronary flow reserve were also examined. RESULTS: Under pharmacological stimulation, higher values of the average peak velocity were observed compared to pacing. A retrograde flow was observed in 8 of 10 patients in the LAD and in 3 of 8 patients in the Cx. The coronary flow reserve was higher under pharmacological stress than during pacing. No relationship was found between the increase of the coronary square plane and the coronary flow reserve. CONCLUSIONS: No decrease in the coronary flow reserve was observed in our patients with HOCM which, however, does not exclude the possibility of ischaemia based on subordinate vessels and microcirculation changes. In the majority of patients a retrograde flow was detected.

[The isolated rabbit heart: comparison between five different modifications]. / Das isolierte Kaninchenherz: ein Vergleich zwischen fünf Varianten.

BACKGROUND: The isolated heart as an experimental model has been firmly established for more than 100 years. MATERIAL AND METHODS: In this study, five modifications are compared: 1. modified Langendorff apparatus (LA) with modified Krebs-Henseleit (KH) solution a) not containing bovine serum albumin (BSA; n = 13) and b) containing BSA (n = 16), 2. LA with KH solution containing BSH and bovine erythrocytes (n = 14), 3. LA with support rabbit (n = 6), and 4. "working heart" preparation with KH solution, BSA and bovine erythrocytes (n = 16). In the latter modification, no balloon was inserted into the left ventricular cavity, i. e., systemic and coronary circuits were not separated from each other. After completion of the preparation and 20-min stabilization, hemodynamic and metabolic data were assessed while the hearts were contracting in the ejecting mode. Thereafter, protocols for different studies were performed that are not presented here. However, the stability of the modifications within their individual protocols is reported. RESULTS: The results suggest that hearts perfused with KH solution are well suited for short protocols. In spite of the additional costs and time, blood perfusion is required for long-lasting protocols or if changes in coronary flow are to be investigated. CONCLUSIONS: The working heart exhibits both the best function and stability at a relatively low experimental expenditure. Yet, it is not suited for studies where perfusion pressure needs to be changed independent of arterial pressure.

Preconditioning: myocardial function and energetics during coronary hypoperfusion and reperfusion.

BACKGROUND: Ischemic preconditioning (IP) is gaining more acceptance as a protective method in beating heart surgery. Yet it remains controversial whether preconditioning can attenuate myocardial dysfunction during reperfusion after severe coronary hypoperfusion. We examined this issue and also the issue of whether this protection is mediated by adenosine A1 receptors. METHODS: In isolated, blood-perfused rabbit hearts, the effects of IP (3 minutes of no flow ischemia and 8 minutes of reperfusion) during 30 minutes of coronary hypoperfusion and 60 minutes of reperfusion were investigated. In two groups (n = 8 each) with and without (control group) preconditioning, ventricular function was assessed by load-insensitive measures: slope of the end-systolic pressure-volume relation (Emax), slope of the stroke work/end-diastolic volume relation (Mw), and end-diastolic pressure-volume relation. External efficiency was calculated, and contractile efficiency was assessed using the reciprocal of the myocardial oxygen consumption-pressure-volume area relationship. To investigate the possible role of adenosine, the adenosine A1 receptor antagonist DPCPX (2.5 micromol/L) was administered before preconditioning in a third group (n = 7). RESULTS: The effects of hypoperfusion on systolic function, diastolic function (dP/dtmin, end-diastolic pressure-volume relation), external efficiency, and contractile efficiency were similar in both the IP and control groups. Lactate efflux was significantly reduced after preconditioning (p = 0.02). During reperfusion, recovery of systolic function and coronary flow were significantly improved in the IP group compared with controls: aortic flow, 85% versus 63% (p = 0.01); dP/dtmax, 91% versus 67% (p = 0.001); pressure-volume area, 97% versus 68% (p = 0.01); Emax, 74% versus 62% (p = 0.03); and Mw, 94% versus 84% (p = 0.04). Release of creatine kinase was reduced in the IP group, 9.6 +/- 1.3 U x 5 min(-1) x 100 g(-1) wet weight, versus controls, 12.7 +/- 2.7 U x 5 min(-1) x 100 g(-1) wet weight (p = 0.04). During reperfusion, contractile efficiency (p = 0.03) and external efficiency (p = 0.02) recovered better in preconditioned than in untreated hearts. Recovery was less pronounced in the DPCPX group compared with the IP group (p, not significant). CONCLUSIONS: The results, derived from load-insensitive measures, confirm that IP provides protection after episodes of severe hypoperfusion by attenuating systolic dysfunction without improving diastolic dysfunction and reduces the severity of anaerobic metabolism as well as ischemic injury. Contractile efficiency and external efficiency both indicate improved energetics after IP (oxygen utilization by the contractile apparatus). The protective effect, at least in part, is mediated by adenosine A1 receptors.