Acute Mitral Regurgitation After Removal of an Impella Device.

Acute mitral regurgitation is a very rare complication of an Impella device. We report a case of a 52-year-old man who had an Impella CP device placed for cardiogenic shock and developed acute mitral regurgitation after removal of the Impella. This was managed with the placement of TandemHeart device.

Right ventricular afterload sensitivity dramatically increases after left ventricular assist device implantation: A multi-center hemodynamic analysis.

BACKGROUND: Right ventricular (RV) failure is a source of morbidity and mortality after left ventricular assist device (LVAD) implantation. In this study we sought to define hemodynamic changes in afterload and RV adaptation to afterload both early after implantation and with prolonged LVAD support. METHODS: We reviewed right heart catheterization (RHC) data from participants who underwent continuous-flow LVAD implantation at our institutions (n = 244), excluding those on inotropic or vasopressor agents, pulmonary vasodilators or additional mechanical support at any RHC assessment. Hemodynamic data were assessed at 5 time intervals: (1) pre-LVAD (within 6 months); (2) early post-LVAD (0 to 6 months); (3) 7 to 12 months; (4) 13 to 18 months; and (5) very late post-LVAD (18 to 36 months). RESULTS: Sixty participants met the inclusion criteria. All measures of right ventricular load (effective arterial elastance, pulmonary vascular compliance and pulmonary vascular resistance) improved between the pre- and early post-LVAD time periods. Despite decreasing load and pulmonary artery wedge pressure (PAWP), RAP remained unchanged and the RAP:PAWP ratio worsened early post-LVAD (0.44 [0.38, 0.63] vs 0.77 [0.59, 1.0], p < 0.001), suggesting a worsening of RV adaptation to load. With continued LVAD support, both RV load and RAP:PAWP decreased in a steep, linear and dependent manner. CONCLUSIONS: Despite reducing RV load, LVAD implantation leads to worsened RV adaptation. With continued LVAD support, both RV afterload and RV adaptation improve, and their relationship remains constant over time post-LVAD. These findings suggest the RV afterload sensitivity increases after LVAD implantation, which has major clinical implications for patients struggling with RV failure.

Adverse neurologic events in patients bridged with long-term mechanical circulatory support: A device-specific comparative analysis.

BACKGROUND: Neurologic complications are among the principal causes of morbidity and mortality after continuous-flow left ventricular assist device (CF-LVAD) implantation. The aim of this study was to describe a focused "real-world" multicenter comparison of neurologic outcomes between HeartMate II (HMII) and HeartWare HVAD CF-LVAD recipients. METHODS: Between March 2009 and October 2014, 497 patients underwent primary CF-LVAD implantation as a bridge to transplantation at centers included in the Mechanical Circulatory Support Research Network; 314 patients (63%) received HMII, and 183 patients (37%) received HVAD. Ischemic cerebrovascular accident, hemorrhagic cerebrovascular accident, and transient ischemic attack were the neurologic outcomes assessed. RESULTS: Median follow-up time for HMII recipients was 0.95 years (0.48, 1.85, range) and for HVAD recipients was 0.44 years (0.19, 0.97, range) (p < 0.001). HMII recipients had significantly fewer neurologic events per patient year for ischemic cerebrovascular accident (0.071) and transient ischemic attack (0.012) compared with HVAD recipients (0.157 and 0.072, respectively). Univariate analysis showed that 51 HMII recipients (16%) had any neurologic event, whereas 34 HVAD recipients (19%) had any neurologic event (p = 0.504). After adjusting for pre-specified covariates (device type, age, sex, atrial fibrillation, diabetes, and Interagency Registry for Mechanically Assisted Circulatory Support profile), multivariable analysis showed only advanced age was able to predict neurologic events (p = 0.02). Neurologic events were comparable between HMII and HVAD recipients after multivariable analysis. CONCLUSIONS: CF-LVAD placement incurs a low but significant risk of neurologic complications in patients receiving CF-LVADs as a bridge to transplantation. Advancing age is a risk factor for any adverse neurologic outcome. This multicenter analysis demonstrated comparable hazard of adverse neurologic events among patients implanted with HMII or HVAD.

Kidney dysfunction and left ventricular assist device support: a comprehensive perioperative review.

Left ventricular assist devices (LVADs) are used increasingly as a bridge to transplantation or as destination therapy in end-stage heart failure patients who do not respond to optimal medical therapy. Many of these patients have end-organ dysfunction, including advanced kidney dysfunction, before and after LVAD implantation. Kidney dysfunction is a marker of adverse outcomes, such as increased morbidity and mortality. This review discusses kidney dysfunction and associated management strategies during the dynamic perioperative time period of LVAD implantation. Furthermore, we suggest potential future research directions to better understand the complex relationship between renal pathophysiology and mechanical circulatory support.

Eosinophilic myocarditis-an unusual cause of left ventricular hypertrophy.

Eosinophilic myocarditis is a rare condition in which inflammation of the heart results in an infiltrative cardiomyopathy that is often difficult to diagnose in the acute setting. It sometimes presents as left ventricular hypertrophy. The authors present a case of a 79-year-old woman with a history of Non-Hodgkin's lymphoma who presented with acute heart failure with marked left ventricular hypertrophy. Echocardiography demonstrated abnormalities consistent with an infiltrative cardiomyopathy, and endomyocardial biopsy showed findings consistent with eosinophilic myocarditis. The patient was managed with diuresis and glucocorticoid therapy, and within 4 weeks of her admission, her clinical status had improved and her echocardiogram normalized. The prompt diagnosis and treatment of this patient's myocarditis likely resulted in her favorable outcome. This illustrates the need for a broad consideration of all the potential causes of hypertrophy and the necessary diagnostic strategies and therapeutic options.

Non-invasive management of vasovagal syncope.

Vasovagal syncope (VVS) is a common disorder of the autonomic nervous system. While recurrent syncope can cause very impaired quality of life, the spells are not generally life-threatening. Both non-pharmacological and pharmacological approaches can be used to treat patients. Conservative management with education, exercise and physical maneuvers, and aggressive volume repletion is adequate for controlling symptoms in most patients. Unfortunately, a minority of patients will continue to have recurrent syncope despite conservative therapy, and they may require medications. These could include vasopressor agents, beta-blockers, or neurohormonal agents. Some patients may require more aggressive device based therapy with pacemakers or radiofrequency ablation, which are emerging therapies for VVS. This paper will review non-procedure based treatments for VVS.

Ongoing clinical trials for Vasovagal Syncope: where are we in 2014?

Vasovagal Syncope (VVS) can lead to a markedly diminished quality of life for some patients. While there are many treatments for this condition including physical, mechanical, pharmacologic, and device-based control of heart rate, there are few that have been shown to be effective in randomized clinical trials. In our local experience, we have achieved significant improvement in symptom frequency and quality of life using algorithms based on the data available and on clinical acumen for the majority of patients with VVS. Despite this, there are still many patients who suffer from treatment refractory VVS. Fortunately, there are a number of ongoing clinical trials that are likely to add to our knowledge. Ongoing clinical trials are reviewed to examine new treatment methods for VVS that were listed on public trial registries as of April 15, 2014. Data from these trials should inform future strategies in the care of patients with VVS.

Medical therapy and physical maneuvers in the treatment of the vasovagal syncope and orthostatic hypotension.

Patients with vasovagal syncope and neurogenic orthostatic hypotension can both present with pre-syncope and syncope resulting from systemic hypotension. While not directly responsible for increased mortality, both of these conditions can have a tremendous deleterious impact on the daily lives of patients. This negative impact can take the form of both physical symptoms and injury, but also a psychological impact from living in fear of the next syncopal episode. Despite these similarities, these are different disorders with fixed damage to the autonomic nerves in neurogenic orthostatic hypotension, as opposed to a transient reflex hypotension in "neurally mediated" vasovagal syncope. The treatment approaches for both disorders are parallel. The first step is to educate the patient about the pathophysiology and prognosis of their disorder. Next, offending medications should be withdrawn when possible. Non-pharmacological therapies and maneuvers can be used, both in an effort to prevent the symptoms and to prevent syncope at the onset of presyncope. This is all that is required in many patients with vasovagal syncope. If needed, pharmacological options are also available for both vasovagal syncope and neurogenic orthostatic hypotension, many of which are focused on blood volume expansion, increasing cardiac venous return, or pressor agents to increase vascular tone. There is a paucity of high-quality clinical trial data to support the use of these pharmacological agents. We aim to review the literature on these different therapy choices and to give recommendations on tailored approaches to the treatment of these conditions.

Desmopressin acutely decreases tachycardia and improves symptoms in the postural tachycardia syndrome.

BACKGROUND: Postural tachycardia syndrome (POTS) induces disabling chronic orthostatic intolerance with an excessive increase in heart rate on standing, and many patients with POTS have low blood volume. Increasing blood volume is a promising approach to this problem. OBJECTIVE: To test the hypothesis that desmopressin (DDAVP) will attenuate the tachycardia and improve symptom burden in patients with POTS. METHODS: In this protocol, patients with POTS (n = 30) underwent acute drug trials with DDAVP 0.2 mg orally and placebo, on separate mornings, in a randomized crossover design. Blood pressure, heart rate, and symptoms were assessed while seated and after standing for up to 10 minutes prior to and hourly for 4 hours following study drug. RESULTS: The standing heart rate was significantly lower following DDAVP than placebo (101.9 ± 14.5 beats/min vs 109.2 ± 17.4 beats/min; P <.001). Standing blood pressure was not affected (P = .28). The symptom burden improved with DDAVP (from a score of 18 ± 18 arbitrary units [AU] to 13 ± 15 AU at 2 hours) compared with placebo (from 18 ± 17 AU to 19 ± 16 AU; P = .010). CONCLUSIONS: Oral DDAVP significantly attenuated tachycardia and improved symptoms in POTS. The safety profile of this approach would need to be examined before it can be recommended for routine treatment of these patients.