Search

Background The prognostic impact of tricuspid regurgitation (TR) following transcatheter aortic valve replacement (TAVR) is uncertain, and the management of patients with severe aortic stenosis and significant TR undergoing TAVR is unclear. Methods Retrospective study investigating the role of TR severity on hospital outcomes in high risk patients with severe aortic stenosis undergoing TAVR. Results A total of 174 participants were included in the present study. The median age was 84 years and 48% were women. The median (IR) STS score was 7.3 (4.7-13.6). The pre-procedural mean (SD) aortic valve area (AVA) was 0.69 (0.2) cm2 and the average (SD) peak and mean gradients were 71 [23]/42 [15] mmHg. Pre TAVR, 28.7% of patients had significant (moderate or severe) TR. Significant TR pre-TAVR increased the risk of in-hospital cardiovascular (CV) and all-cause and mortality [adjusted relative risk (RR) (95% CI): 14.67 (1.35-159.51) and 5.09 (1.14-22.72), respectively], and those with severe TR post-TAVR had longer hospital stay [median (IR): 9.9 (2.9-17.0) days]. No improvement or worsened TR (greater than mild) post-TAVR was associated with higher CV and all-cause mortality [adjusted RR (95% CI): 21.5 (1.81-255.96) and 8.19 (1.67-40.29), respectively]. Right ventricular systolic pressure (RVSP) was independently associated with TR severity pre and post TAVR. Conclusions Significant TR was common among patients undergoing high risk TAVR, and is associated with increased in hospital mortality and longer hospital stay. Patients with elevated RVSP and persistent moderate or severe TR after TAVR are at higher risk of in hospital death.

BACKGROUND Post-myocardial infarction (MI) ventricular septal defects (PIVSD) are an uncommon but life-threatening complication of acute MI. Although surgical closure has been the standard of care, mortality, and recurrence of VSD remain high even after emergent surgery. Transcatheter VSD closure (TCC) devices have become an alternative or adjunct to surgical closure. METHODS Online database search was performed for studies that included adults with PIVSD who underwent medical treatment (MT) alone, surgical closure (SC) (early or late), and TCC (early, late, or for post-surgical residual VSD). RESULTS Twenty-six studies were included with a total of 737 patients who underwent either MT (N = 100), SC (early (n = 167), late (n = 100)), and TCC (early (n = 176), late (n = 115), or post-surgical residual VSD (n = 79)). The 30-day mortality among MT group was 92 ± 6.3%, among SC was 61 ± 22.5% (early 56 ± 23%, late 41 ± 30%), and for all TCC patients was 33 ± 24% (early 54 ± 32.7%, late 16 ± 26%), and TCC for post-surgical residual VSD 11 ± 34.9%. The mortality among overall SC, overall TCC and early TCC groups was significantly lower as compared with the MT (P

Introduction Patients with acute heart failure (AHF) & acute kidney injury (AKI) have increased hospital mortality and readmissions. The impact of atrial fibrillation (AF) in these patients has not been well studied. We examined the hypothesis that the presence of AF in patients with AHF and AKI will further increase mortality and rates of readmission. Methods Medical records of patients who were admitted with AHF and AKI between 2008 and 2010 (n=244) were reviewed. The patients were divided into two groups: patients with AHF and AKI with presence of AF (N= 66), and absence of AF (N=178). Presence of AF was confirmed using electrocardiogram on admission. AKI was defined as a rise of serum creatinine > 0.3 mg/dL above their baseline. Results We studied 244 patients with AHF and AKI (121 male and 123 female) with a mean age of 64.12 ±16.4; 27 % of patients had AF on admission. The 30 days in-hospital mortality, 90-days readmission and length of hospital stay were significantly higher in patients with AF compared to patients without AF (Table 1). In the multivariate logistic regression model the only independent predictors of mortality were left ventricular ejection fraction (odds ratio 0.963; 95 % CI 0.930 to 0.997; P = 0.032) and the use of angiotensin converting enzyme inhibitors (odds ratio 0.225; 95 % CI 0.066 to 0.763; P = 0.017). Conclusions The presence of AF in patients with AHF and AKI is associated with increased mortality, readmission rates and length of hospital stay. Higher LVEF and the use of ACE inhibitors predicted better survival.

Drugs, including those used during diagnostic procedures, can have adverse effects and potentially serious side-effects, especially in complicated patients with significant comorbidity. Benzocaine is frequently used as an oropharyngeal anesthetic agent during bronchoscopy, transesophageal echocardiography, and upper GI endoscopy and can cause methemoglobinemia, a potentially life-threatening event if not diagnosed and treated quickly. Co-oximetry is the gold standard for the diagnosis of methemoglobinemia and can quantitate blood levels, which in turn correlate with the clinical presentation and the urgency for treatment. Methylene blue is the treatment of choice for methemoglobinemia. In this case report we discuss the pathophysiology, the clinical presentation, the diagnosis, and the treatment of benzocaine-induced methemoglobinemia.

We are reporting a case of familial thoracic aortic aneurysm and dissection in a 26-year-old man with no significant past medical history and a family history of dissecting aortic aneurysm in his mother at the age of 40. The patient presented with cough, shortness of breath, and chest pain. Chest X-ray showed bilateral pulmonary infiltrates. CT scan of the chest showed a dissection of the ascending aorta. The patient underwent aortic dissection repair and three months later he returned to our hospital with new complaints of back pain. CT angiography showed a new aortic dissection extending from the left carotid artery through the bifurcation and into the iliac arteries. The patient underwent replacement of the aortic root, ascending aorta, total aortic arch, and aortic valve. The patient recovered well postoperatively. Genetic studies of the patient and his children revealed no mutations in ACTA2, TGFBR1, TGFBR2, TGFB2, MYH11, MYLK, SMAD3, or FBN1. This case report focuses on a patient with familial TAAD and discusses the associated genetic loci and available screening methods. It is important to recognize potential cases of familial TAAD and understand the available screening methods since early diagnosis allows appropriate management of risk factors and treatment when necessary.

Partial and generalized seizures often affect autonomic functions during seizures, and interictal and postictal periods. We investigated possible interictal electrocardiographic abnormalities in patients with generalized tonic-clonic seizures (GTCS), together with evaluating any structural heart changes by echocardiography in these patients in comparison with healthy controls. We studied 120 definite GTCS patients (76 males and 44 females) who are neither diabetic nor under any medical treatment, and 60 healthy controls with a mean age of 25.2 ± 9.3 and 27.3 ± 7.5 years; respectively. Resting systolic and diastolic arterial blood pressures were measured, and standard 12-lead electrocardiograms and a 2-dimensional echocardiographic examination were performed. In univariate analysis, GTCS patients (compared to controls) had significantly lower means of PR interval (147.2 ± 18.6 versus 153.8 ± 22.6 msec; P = 0.037), QT interval (362.8 ± 22.9 versus 379.9 ± 29.3 msec; P < 0.001), and QTc interval (425.5 ± 20.7 versus 441.6 ± 19.9 msec; P < 0.001) but significantly higher mean left atrial diameter (3.49 ± 0.64 versus 3.09 ± 0.45 cm; P < 0.001). After adjusting for age, gender, and body mass index in a multivariate adjusted logistic regression model, left atrial diameter (OR = 3.941 [1.739 - 8.932]) and QTc (OR = 0.924 [0.895 - 0.954]) were significantly and independently associated with GTCS. In conclusion, patients with epilepsy may be predisposed to disturbances of autonomic functions with subsequent cardiac arrhythmias due to the effects of recurrent seizures on cardiac microstructure. Further work is needed to stratify the risk of sudden unexplained cardiac death (SUDEP) on the basis of interictal autonomic parameters to improve prognosis.

Tricuspid regurgitation (TR) may lessen the potential benefits of TAVR. We aimed to investigate the impact of TR on TAVR outcomes and to ascertain factors associated with TR severity. Patients with severe aortic stenosis that underwent TAVR at MSMC, Miami Beach, FL from August, 1st 2014 to January

Vasoplegia syndrome is a well known complication after cardiac surgery and has a significant morbidity and mortality. It is characterized by profound vasodilation and loss of systemic vascular resistance leading to hypotension. The pathogenesis of vasoplegia involves the activation of contact, coagulation and complement systems and the activation of leukocytes, platelets and endothelial cells resulting in an imbalance in the regulation of the vascular tone leading to postcardiac surgery vasoplegia. Multiple risk factors have been identified that help predict vasoplegia. Treatment requires mainly vasopressors, but hypotension can be refractory to vasopressors. Some studies suggest that methylene blue can reverse refractory hypotension in these patients and may prevent the development of the syndrome, but more studies are needed with this drug. In this review, we will discuss the pathophysiology of the vasoplegia syndrome and associated risk factors for this complication and briefly outline current therapeutic strategies.

Acute kidney injury (AKI) is a common complication among patients with acute heart failure (AHF) (30%) and is associated with increased in-hospital mortality and readmission. Limited data are available about the impact of left ventricular systolic function on the prognosis of these patients.

Background: Volume contraction frequently contributes to the development of acute kidney injury. The rapid assessment of volume status in patients with acute kidney injury could improve decision making and outcomes. Methods: The maximum and minimum diameters and percent collapsibility of the inferior vena cava (IVC) were measured in 30 patients admitted to the medical intensive care unit with laboratory evidence of acute kidney injury. These measurements were made on the day of admission and 24 hours following admission. Information about age, gender, body mass index, serum creatinine levels, and fluid balances was recorded. Results: This study included 30 patients with a mean age is 62.4 ±16.0 years. The mean initial creatinine was 4.3 ± 4.2 mg/dL (range: 1.7 mg/dL to 22.1 mg/dL). The mean fractional excretion of sodium was 2.06 ± 2.65%. The mean maximum diameter of inferior vena cava was 1.8 ± 0.5 cm with the range is 0.4-2.65 cm. The mean percent collapse was 32 ± 20%. Five patients had evidence of hypovolemia using guidelines from the American Society of Echocardiology; 6 patients had evidence of hypervolemia. Nineteen patients had measurements between these 2 categories. There is no significant change in mean diameters following fluid administration for 24 hours. An initial IVC diameter of 0.94 cm predicted ≥ 30% collapsibility with an area under the curve is 0.748. Discussion: Patients with acute kidney injury based on laboratory measurements had evidence for hypovolemia, euvolemia, and hypervolemia based on IVC measurements. There was no consistent change in IVC dimensions following fluid administration, even though the creatinine fell in most patients. Simple bedside measurements of IVC dimensions can facilitate fluid administration decisions but must be used with clinical assessment.

Muscle regeneration depends on satellite cells (SCs), quiescent precursors that, in consequence of injury or in pathological states such as muscular dystrophies, activate, proliferate, and differentiate to repair the damaged tissue. A subset of SCs undergoes self-renewal, thus preserving the SC pool and its regenerative potential. Unacylated ghrelin (UnAG) is a circulating hormone that protects muscle from atrophy, promotes myoblast differentiation, and enhances ischemia-induced muscle regeneration. Here we show that UnAG increases SC activity and stimulates Par polarity complex/p38-mediated asymmetric division, fostering both SC self-renewal and myoblast differentiation. Because of those activities on different steps of muscle regeneration, we hypothesized a beneficial effect of UnAG in mdx dystrophic mice, in which the absence of dystrophin leads to chronic muscle degeneration, defective muscle regeneration, fibrosis, and, at later stages of the pathology, SC pool exhaustion. Upregulation of UnAG levels in mdx mice reduces muscle degeneration, improves muscle function, and increases dystrophin-null SC self-renewal, maintaining the SC pool. Our results suggest that UnAG has significant therapeutic potential for preserving the muscles in dystrophies.