Sharon Rubin

Pharmacologic therapy of chronic heart failure.

Over the past 2 decades, investigators have learned more about the pathophysiologic changes that occur in systolic and diastolic dysfunction. Ironically, in some cases, the biologic pathways that have protected the heart during acute dysfunction are the same pathways that cause progressive deleterious effects with chronic activation. In particular, it is the activation of the neurohormonal system that has a significant impact on disease progression. As a result, the neurohormonal system has provided a key target for pharmacologic therapy in patients with heart failure secondary to systolic dysfunction. These targets include the renin-angiotensin-aldosterone system as well as the sympathetic nervous system. Neurohormonal manipulation, however, is often ineffective in the pharmacologic therapy of patients with endstage heart failure, therefore other treatment strategies — including the use of inotropic agents to improve pump function and diuretics to control fluid balance are needed.

Renal dysfunction in heart failure patients: what is the evidence?

Congestive heart failure (CHF) is an increasingly common medical condition and the fastest growing cardiovascular diagnosis in North America. Over one-third of patients with heart failure also have renal insufficiency. It has been shown that renal insufficiency confers worsened outcomes to patients with heart failure. However, a majority of the larger and therapy-defining heart failure medication and device trials exclude patients with advanced renal dysfunction. These studies also infrequently perform subgroup analyses based on the degree of renal dysfunction. The lack of information on heart failure patients who have renal insufficiency likely contributes to their being prescribed mortality and morbidity reducing medications and receiving diagnostic and therapeutic procedures at lower rates than heart failure patients with normal renal function. Inclusion of patients with renal insufficiency in heart failure studies and published guidelines for medication, device, and interventional therapies would likely improve patient outcomes.

Photoplethysmographic Signal to Screen Sleep-Disordered Breathing in Hospitalized Heart Failure Patients: Feasibility of a Prospective Clinical Pathway.

OBJECTIVES The purpose of this study was to evaluate the plethysmographic signal-derived oxygen desaturation index (ODI) as an inpatient screening strategy to identify sleep-disordered breathing (SDB) in patients with congestive heart failure (CHF). BACKGROUND SDB is highly prevalent among patients hospitalized with CHF but is widely underdiagnosed. We evaluated overnight photoplethysmography as a possible screening strategy for hospitalized patients with CHF. METHODS Consecutively admitted heart failure patients with high clinical suspicion of SDB and ODI ≥5 were offered outpatient polysomnography (PSG), which was completed within 4 weeks of discharge. PSG was considered positive if the apnea hypoxia index (AHI) was ≥5. A Bland-Altman plot was used to assess agreement between ODI and AHI. Receiver-operator characteristics were determined for ODI ≥5 and AHI ≥5. RESULTS A screening questionnaire identified 246 of 282 consecutive patients with positive symptoms for SDB. Of these patients, 105 patients were offered further evaluation and 86 had ODI ≥5 (mean ODI 17 ± 17). Among these 86 patients, 68 underwent outpatient PSG within 4 weeks of discharge. PSG showed that 64 (94%) had SDB, with a mean AHI of 28. Inpatient ODI correlated well with PSG-derived AHI. The area under the curve was 0.82 for AHI ≥5. The Bland-Altman plot revealed no major bias. Matthews correlation coefficient revealed that the optimal cut-off for ODI is 5. CONCLUSIONS Screening hospitalized patients with heart failure using targeted inpatient ODI identifies a cohort of patients with a high prevalence of SDB. Our screening strategy provides a potentially cost-effective method for early detection and treatment of SDB.

Inappropriate sinus tachycardia in a transplanted heart—Further insights into pathogenesis

Inappropriate sinus tachycardia (IST) is relatively uncommon and poorly understood. Proposed mechanisms include sympathovagal imbalance or a primary sinus node (SAN) abnormality. We report a case of IST in a transplanted heart refractory to pharmacological therapy and causing severe allograft dysfunction. Secondary causes of sinus tachycardia were excluded. Cardiomyopathy resolved with heart rate (HR) control by SAN modification and -blocker therapy. The occurrence of IST in a completely denervated heart excluded a sympathovagal mechanism and implicated a primary defect in the donor SAN.

Recurrent orthostatic syncope due to left atrial and left ventricular collapse after a continuous-flow left ventricular assist device implantation

Left ventricular assist devices (LVADs) have become an established treatment for patients with advanced heart failure as a bridge to transplantation or for permanent support as an alternative to heart transplantation. Continuous-flow LVADs have been shown to improve outcomes, including survival, and reduce device failure compared with pulsatile devices. Although LVADs have been shown to be a good option for patients with end-stage heart failure, unanticipated complications may occur. We describe dynamic left atrial and left ventricular chamber collapse related to postural changes in a patient with a recent continuous-flow LVAD implantation.

TREATMENT OF SLEEP DISORDERED BREATHING IN PATIENTS ADMITTED FOR DECOMPENSATED HEART FAILURE REDUCES 6 MONTHS HOSPITAL VISITS

Despite outcome improvement re-hospitalization of congestive heart failure (CHF) is high. Sleep disordered breathing (SDB) is common and under-diagnosed in CHF patients. We hypothesized that early recognition and treatment of SDB in hospitalized CHF patients will reduce hospital visits (combined end