Current Cardiology Reports

The purpose of this review is to highlight the past impact and current role of the Appropriate Use Criteria (AUC) for echocardiography in value-based healthcare, and to address future implications in light of the recent mandate from the Centers for Medicare and Medicaid Services to incorporate AUC for other imaging modalities. Several studies have proven that the AUC effectively stratify the clinical practice of echocardiography as they predict important echo abnormalities and impact optimal patient care. Recent investigations have tested new technologies and demonstrated the feasibility and scalability of the application of the AUC for echocardiography at the point of care. The AUC for echocardiography has accomplished their core mission, as utilization has moderated over the last decade and mandatory implementation at the point of care for echocardiography remains rare. While a new mandate signals another wave of focus on appropriate utilization, echocardiography stands ready.

It is well established that strict glycemic control for the hospitalized stroke patient is associated with improved outcome compared with poor control. This is particularly true for the stroke patients because hyperglycemia can adversely affect ischemic damage. A blood sugar level of less than 110 mg/dL is recommended for critically ill patients and should be achieved by intravenous insulin administration in an intensive care unit setting. Many stroke patients are unable to swallow, and insulin requirement must be readjusted carefully to conform to the nutritional state of the patient. The transition from intravenous insulin to subcutaneous insulin or oral antihyperglycemic agents must be carefully monitored. Careful discharge planning of diabetic care for the stroke patient is necessary to prevent long-term sequelae of inadequate control.

Most patients with ischemic stroke or transient ischemic attack are screened for internal carotid artery stenosis. Although it is important to identify candidates for endarterectomy or stenting, the clinician must realize that most patients are not candidates for revascularization. Therefore, medical therapy remains the cornerstone of treatment. In this article, current thinking on medical therapy for carotid atherosclerosis is outlined, including aggressive use of statins, targeted blood pressure lowering, and antithrombotic therapy. Implementation of these therapies will likely reduce the need for revascularization procedures in the future.

Despite recent favorable trends in survival, heart failure remains a highly fatal disease. Improvements in the prevention of early death from coronary artery disease, along with an aging population, have resulted in an increased prevalence for heart failure in the United States. In the management of patients with heart failure secondary to coronary artery disease, the relative efficacy of invasive therapies such as coronary revascularization, surgical left ventricle remodeling, internal cardiac defibrillator implantation, cardioverter resynchronization therapy, mechanical ventricular assist, and cardiac transplantation need to be considered. Clinical studies examining these important treatment options are reviewed in order to better define the optimal management strategy for this challenging population of patients.

Substantial progress has been made in understanding the pathophysiology of regional and global left ventricular (LV) dysfunction and the states of hibernation and stunning in patients with heart failure. The clinical literature on the use of noninvasive imaging to assess myocardial viability has evolved from predicting improvement in regional LV function to predicting patient-related outcomes, including heart failure symptom improvement and survival after revascularization. A substantial body of observational cohort data demonstrates that mortality risk is high in patients with coronary artery disease and LV dysfunction who have substantial viable myocardium, and that risk is reduced by revascularization. Thus, noninvasive imaging of myocardial ischemia and viability can provide important prognostic information in patients with heart failure and LV dysfunction, and provide a signal of the potential benefit of revascularization.

Kidney disease may be the cause or a consequence of hypertension. Hypertension affects 25% of the adult population in the United States. Similarly, chronic kidney disease (CKD) and end-stage renal disease (ESRD) have been steadily increasing in incidence because of the increasing age of the US population and rise in the incidence of risk factors, including hypertension. Substantial evidence supports the notion that elevated blood pressure is the most significant risk factor for the development of CKD. Microalbuminuria has been shown to be the early marker of hypertensive renal disease. Furthermore, therapy to reduce microalbuminuria was associated with delay in the progression of renal disease. Black Americans are at higher risk for developing hypertensive nephrosclerosis than whites. Hypertension is a major risk factor for cardiovascular events in patients with CKD and ESRD and those who have undergone renal transplantation. Studies have documented that elevated serum creatinine and CKD are risk factors for a cardiovascular event. Tight blood pressure control has been shown to reduce microalbuminuria and proteinuria and to delay progression of renal disease. Tailoring the choice of antihypertensive medication to the clinical setting to achieve a blood pressure goal is critical in reducing complications from this deadly connection.

Despite the higher incidence of paravalvular regurgitation (PVR) with transcatheter aortic valve replacement (TAVR), this novel treatment modality has rapidly emerged as a reasonable alternative to surgical aortic valve replacement (SAVR) in high risk and inoperable patients. This review will discuss the current literature with respect to assessment, outcomes, predictors, and intraprocedural treatment options of PVR following TAVR. Understanding the predictors may help reduce the incidence of PVR and improving the outcome of this procedure.

Congenital heart disease (CHD) is the most frequently occurring birth defect. Majority of the earlier reviews focussed on the association of genetic factors with CHD. A few epidemiological studies provide convincing evidence for environmental factors in the causation of CHD. Although the multifactorial theory of gene-environment interaction is the prevailing explanation, explicit understanding of the biological mechanism(s) involved, remains obscure. Nonetheless, integration of all the information into one platform would enable us to better understand the collective risk implicated in CHD development. Great strides in novel genomic technologies namely, massive parallel sequencing, whole exome sequencing, multiomics studies supported by system-biology have greatly improved our understanding of the aetiology of CHD. Molecular genetic studies reveal that cardiac specific gene variants in transcription factors or signalling molecules, or structural proteins could cause CHD. Additionally, non-hereditary contributors such as exposure to teratogens, maternal nutrition, parental age and lifestyle factors also contribute to induce CHD. Moreover, DNA methylation and non-coding RNA are also correlated with CHD. Here, we inform that a complex combination of genetic, environmental and epigenetic factors interact to interfere with morphogenetic processes of cardiac development leading to CHD. It is important, not only to identify individual genetic and non-inherited risk factors but also to recognize which factors interact mutually, causing cardiac defects.