Preclinical cardiac disease in nonalcoholic fatty liver disease with and without metabolic syndrome.

BACKGROUND: Metabolic syndrome is associated with preclinical cardiac disease and nonalcoholic fatty liver disease (NAFLD). It is uncertain whether preclinical cardiac disease is present in patients with NAFLD without metabolic syndrome (MetS). OBJECTIVE: To explore preclinical cardiac disease in patients with NAFLD. METHODS: A total of 64 patients with NAFLD, based on computed tomography scans liver attenuation, were identified. A control group, matched to age and gender, comprising of 94 patients was also drafted. Finally, two additional groups of patients with metabolic syndrome, with (n = 40) and without (n = 74) NAFLD, were also identified. Patients with hypertension, diabetes mellitus, and other concomitant liver diseases were excluded from the NAFLD group. Echocardiograms of all groups were reviewed. RESULTS: Severe NAFLD compared to control was associated with a higher left ventricular mass after normalization for height2.7 (LVMHt2.7) (95% CI = 0.39, 12.92) and lower ratio of peak "E" (early) and "A" (late) diastolic ventricular filling velocities (E/A) - 0.39 (95% CI = -0.58, -0.19). Patients with metabolic syndrome (95% CI = 0.02, 0.09), metabolic syndrome with NAFLD (95% CI = 0.02, 0.08), or severe NAFLD (95% CI = 0.02, 0.09) compared to control was associated with a higher relative wall thickness (RWT). CONCLUSION: Healthy adults with NAFLD without metabolic syndrome, after adjusting for body mass index, demonstrated significant echocardiographic changes. Our results show that NAFLD is associated with preclinical cardiac disease, and this association is independent of traditional risk factors like systemic hypertension and diabetes mellitus.

A Case of Isolated Left Ventricular Non-Compaction Cardiomyopathy in a HIV Patient Presenting With Acute Heart Failure.

The etiology of cardiomyopathy in a HIV patient is multifactorial. Identifying the etiology of cardiomyopathy in a HIV patient needs extensive evaluation. Common causes include ischemic cardiomyopathy, myocarditis due to viral infections and opportunistic infections, cocaine abuse, alcoholic heart disease, drug toxicity or due to nutritional deficiencies. However, in a number of cases the etiology is unknown. We report a case of 36-year-old African American man with history of HIV who presented with acute heart failure due to left ventricular non-compaction (LVNC). Transthoracic and transesophageal echocardiogram showed significant left ventricular trabeculations and blood flow in deep recesses. Endomyocardial biopsy was suggestive of LVNC. He underwent left ventricular assist device implantation for destination therapy and subsequently cardiac transplantation. The diagnosis of LVNC is often made by echocardiogram. As LVNC could be a normal variant, a comprehensive diagnostic assessment including multimodality imaging, a systematic screening of first degree relatives, and a comprehensive clinical and genetic assessment by a multidisciplinary team may be needed to arrive at the diagnosis. Early diagnosis and timely intervention may reduce the risk of premature death in these young patients.

Inhaled Nitric Oxide as an Adjunct to Thrombolytic Therapy in a Patient with Submassive Pulmonary Embolism and Severe Hypoxemia.

INTRODUCTION: Inhaled nitric oxide (iNO) is a selective pulmonary vasodilator with limited indications in adults. We present a patient with hypoxemia and right ventricular dysfunction due to submassive acute pulmonary emboli where iNO was used as a bridge to thrombolysis. CASE: A 29-year-old male was admitted to the intensive care unit (ICU) for alcohol intoxication complicated with aspiration pneumonia and acute respiratory failure requiring mechanical ventilation. His medical history included morbid obesity (BMI 43) and alcohol dependence syndrome. Nine days after admission, he developed severe acute hypoxia and tachycardia with arterial oxygen tension (PaO2) of 52 mmHg requiring a positive end-expiratory pressure (PEEP) of 14 cmH2O and fraction of inspired oxygen (FiO2) of 1. Chest computed tomography (CT) revealed a large embolus in the right main pulmonary artery and transthoracic echocardiogram (TTE) reported new right ventricular dilatation with decreased right ventricular function. Due to the severe hypoxemia, he was started on iNO via the breathing circuit of the ventilator at a concentration of 20 parts per million (ppm) with steady improvement in oxygenation after 1 hour with a PaO2 of 81 mmHg on the same ventilator setting. The patient was given thrombolysis with alteplase and the iNO was slowly tapered off during the subsequent four days with concomitant successful tapering of PEEP to 8 cmH2O and FiO2 of 0.45. CONCLUSION: Inhaled NO has been used to improve ventilation-perfusion matching and also to reduce pulmonary vascular resistance (PVR). Its effects on PVR may be useful in the setting of acute pulmonary emboli where vascular obstruction and vasoconstriction contribute to increased pulmonary arterial pressure and PVR which can present as acute right heart failure. We suggest that iNO, if available, could be considered in those patients with acute pulmonary emboli associated with significant hypoxemia as an adjunctive therapy or bridge to thrombolysis or thrombectomy.

The metabolic model of heart failure: the role of sodium glucose co-transporter-2 (SGLT-2) inhibition.

Heart failure (HF) is one of the leading causes of hospital readmissions and health care expenditures. With a vast degree of advancements in the clinical approach and diagnosis, its management protocol is limited in terms of enhancing quality of life and prognosis. Type 2 diabetes mellitus (T2DM) is considered as one of the commonly associated comorbid conditions in the HF population. The understanding of the molecular and metabolic models of HF has led to the utilization of therapeutic goals of T2DM in improving HF-related complications. In the recent era, SGLT-2 inhibitors have shown success in decreasing cardiovascular mortality in the T2DM population. This article will help the reviewer to comprehend the pathophysiology of HF and the potential role of SGLT-2 inhibitors in the management algorithm of HF and its associated risk factors in T2DM.

An Unusual Case of Ototoxicity with Use of Oral Vancomycin.

INTRODUCTION: Systemic absorption of oral vancomycin is poor due to the size of the molecule and its pharmacokinetics. It has an elimination half life of 5-11 hours in patients with normal renal function. We present a rare case of ototoxicity after oral vancomycin administration and detectable serum vancomycin levels 24 hours after cessation of vancomycin. CASE PRESENTATION: A 42-year-old woman with a history of hypertension, diabetes mellitus, and previously treated Clostridium difficile colitis presented with abdominal pain and diarrhea for two weeks. Clostridium difficile infection was confirmed by PCR, and at the time of diagnosis and initiation of therapy, the patient had normal renal function. Vancomycin was initiated at a dose of 125 mg po q6h. After the third dose of oral vancomycin, the patient reported new symptoms of lightheadedness, sensations of "buzzing" and whistling of bilateral ears, and decreased perception of hearing described as "clogged ears." The patient reported to the emergency department the next day due to worsening of these symptoms, and vancomycin dosing was reduced to every 8 hours; however, the patient reported the auditory symptoms persisted. On day three, vancomycin was discontinued with gradual resolution of symptoms over the next 12 hours. On day four, a serum random vancomycin level obtained 24 hours after the last dose was detectable at 2 mcg/dl. Temporal association of the patient's symptoms and improvement with cessation of therapy along with a detectable vancomycin level indicates systemic absorption of oral vancomycin with subsequent ototoxicity. DISCUSSION: The potential for absorption of oral vancomycin is not well described and is attributed to compromised intestinal epithelium allowing for increased drug absorption. Few studies suggested that oral vancomycin may result in therapeutic or even potentially toxic levels of serum vancomycin in patients with impaired renal function. Ototoxicity may be a transient or permanent side effect of vancomycin therapy and is related to high serum levels. Symptoms usually resolve after decreasing the dose or cessation of vancomycin. No detectable serum vancomycin levels were found in 98% of the patients treated with oral vancomycin in a prospective study. The described case is unusual because despite normal renal function, the patient still developed ototoxicity, and systemic absorption of the drug was confirmed with a measurable vancomycin level approximately 24 hours after the drug was stopped. Additionally, the only other medication prescribed to the patient at the time of vancomycin administration was metformin at a dose of 500 mg po bid which has no known idiosyncratic interactions potentiating adverse side effects to vancomycin. This case reflects that some patients may be more susceptible to increased systemic absorption via the oral route, and the possibility for ototoxicity should be considered and discussed with patients while prescribing oral vancomycin.