Optimizer Smart System for the treatment of chronic heart failure: Overview of its safety and efficacy.

Introduction: Heart failure (HF) is a major cause of morbidity and mortality throughout the world. Despite the significant progress in the prevention and treatment of HF, mortality rates still remain high. Device therapy for HF includes cardiac resynchronization therapy (CRT) and the use of an implantable cardioverter-defibrillator (ICD). Recently, a new device therapy for the treatment of HF became available, called cardiac contractility modulation (CCM). CCM is a new device therapy for patients with HF who do not qualify for CRT. It is implanted in a minimally invasive manner to improve the patient's morbidity. Optimizer Smart System is a new device that delivers CCM therapy.Areas covered: We review the function of the Optimizer Smart System, the data from the recent clinical trials, and discuss its efficacy and future projections in the treatment for HF.Expert opinion: CCM therapy provided with the Optimizer® Smart System is safe, feasible, and applicable to a wide range of patients with HF. To demonstrate the effectiveness of the Optimizer Smart System's use merits further large multicenter randomized controlled trials.

Usefulness of Serum Triiodothyronine (T3) to Predict Outcomes in Patients Hospitalized With Acute Heart Failure.

Thyroid hormone plays an important role in cardiac function. Low levels of serum triiodothyronine (T3) due to nonthyroidal illness syndrome may have adverse effects in heart failure (HF). This study was designed to assess the ability of T3 to predict in-hospital outcomes in patients with acute HF. In total, 137 patients without thyroid disease or treatment with drugs which affect TH levels, who were hospitalized with acute HF were prospectively enrolled and studied. TH levels were tested upon hospital admission, and outcomes were compared between patients with low (<2.3 pg/ml) and normal (≥2.3 pg/ml) free T3 levels as well as between those with low (<0.6 ng/ml) and normal (≥0.6 ng/ml) total T3 levels. Low free T3 correlated with an increased length of stay in the hospital (median 11 vs 7 days, p <0.001) and higher rates of intensive care unit admission (31.8% vs 16.9%, p = 0.047), with a trend toward increased need for invasive mechanical ventilation (9.0% vs 1.4%, p = 0.056). Low total T3 correlated with an increased length of stay in the hospital (median 11 vs 7 days, p <0.001) and increased need for invasive mechanical ventilation (9.8% vs 1.3%, p = 0.045). In conclusion, low T3 predicts worse hospital outcomes in patients with acute HF and can be useful in the risk stratification of these patients.

Brief sympathetic activation precedes the development of ventricular tachycardia and ventricular fibrillation in hibernating myocardium.

BACKGROUND: Hibernating myocardium develops inhomogeneity in myocardial sympathetic innervation with spontaneous sudden cardiac death (SCD) because of ventricular fibrillation (VF). The triggers and prodromal arrhythmias initiating SCD in this substrate are unknown. METHODS: Swine chronically instrumented with a proximal left anterior descending coronary artery stenosis underwent placement of an implantable telemetry unit capable of continuously recording digitized electrocardiogram and left ventricular pressure signals at 1 kHz in conscious unrestrained animals for periods of up to 5 months. RESULTS: Spontaneous SCD (n = 10) was initiated by a close-coupled premature ventricular contraction followed by ventricular tachycardia (VT) that degenerated into VF during brief sympathetic activation. Peak heart rates were similar in animals that developed SCD vs survivors (250 +/- 12 vs 261 +/- 6 bpm). Electrocardiogram evidence of ischemia preceding VT/VF occurred in only 1 animal, and there was no significant infarction. CONCLUSIONS: Spontaneous VT/VF in hibernating myocardium develops during brief sympathetic activation with only rare evidence of acute ischemia. This supports the notion that the regional remodeling accompanying hibernating myocardium may be a novel substrate for the development of SCD in chronic ischemic heart disease.

Contrast echocardiography improves the diagnostic yield of transthoracic studies performed in the intensive care setting by novice sonographers.

BACKGROUND: Bedside portable echocardiography in the intensive care department (ICU) is technically difficult, but crucial for directing patient care. Prior studies have shown contrast echocardiography (CE) in the ICU clarifies left ventricular wall motion when performed by experienced sonographers (ESO). However, in most hospitals, ESO are unavailable around the clock, and less experienced cardiovascular fellows or trainees may be asked to perform these examinations. METHODS: Transthoracic echocardiograms were retrospectively evaluated by level III trained echocardiographers for 213 patients in the ICU. Most were performed to assess left ventricular function (65% or 139 of 213) and were scanned by cardiology fellows (70% or 149 of 213) with less than 3 months echocardiography experience. Contrast agent was used in 29% (62 of 213) of all patients. RESULTS: The conversion of suboptimal or diagnostically inadequate apical 4- and 2-chamber views to diagnostically adequate with contrast was statistically significant when performed by both cardiology fellows and ESO (Fischer exact test, P < .0002). CONCLUSIONS: CE is effective in improving the diagnostic yield of transthoracic echocardiographic ICU studies performed by both novice sonographers and ESO. Using cardiology fellows to perform CE in this setting can be appropriate, particularly in after-hour situations, when ESO are not always available and the clinical question is left ventricular function. Results also suggest cardiology fellows can easily learn CE.

Assessment of intracardiac anomalies in two adults with Ivemark's syndrome.

Ivemark's syndrome consists of intracardiac anomalies, abnormal lobation of the lungs, and abdominal heterotaxy. A frequent intracardiac anomaly seen in Ivemark's syndrome is a common atrium, which is associated with left-to-right shunting. The increased blood flow and resistance within the pulmonary vasculature creates pulmonary hypertension and eventual reversal of the shunt physiology. In the absence of additional cyanotic malformations, survival into adulthood without prior surgical septation of the common atrium depends on the extent of pulmonary hypertension and intracardiac right-to-left shunting. We present two patients with a common atrium in the setting of Ivemark's syndrome who survived into adulthood without prior operation. Two-dimensional echocardiography assessed their intracardiac structures. One patient had right atrial isomerism manifested by asplenia and a common atrium, into which the hepatic veins drained directly, and the other patient had left atrial isomerism manifested by polysplenia, a common atrium, and a ventricular septal defect with a single atrioventricular valve. Neither patient had additional cyanotic malformations, including obstruction to pulmonary venous return, transposition of the great vessels, or pulmonic valve stenosis. The 2-dimensional echocardiogram guides the clinician to refer patients for surgical septation of the common atrium before the right-to-left shunt physiology predominates. The medical and surgical treatment of these patients is discussed.