Current Treatment Options in Cardiovascular Medicine最新文献

Purpose of review: To review the current evidence and ongoing clinical trials evaluating the efficacy and safety of tenecteplase (TNK), an alternative tissue plasminogen activator (tPA), in the acute management of arterial ischemic stroke (AIS). To date, alteplase is the only tPA approved by the United States FDA for use in AIS.

Recent findings: There have been multiple phase two and three trials investigating the safety and efficacy of TNK in AIS. In patients with AIS due to large vessel occlusion, one randomized controlled trial demonstrated superiority of TNK for vessel recanalization rates and long-term functional outcomes when compared to alteplase. A meta-analysis of all phase two and three trials evaluating TNK in AIS concluded that TNK has a comparable safety and efficacy profile to alteplase. The results of these trials prompted new recommendations in the Acute Stroke Guideline published by the AHA suggesting it may be reasonable to use as an alternative to alteplase. Furthermore, recent real-world data has also reported decreased door-to-needle time with TNK utilization.

Summary: In patients with AIS, use of a thrombolytic agent is standard of care and has been shown to reduce neurological disability and improve functional outcome. Randomized controlled trials have demonstrated that TNK is non-inferior to alteplase from a clinical outcome and safety standpoint. The existing data evaluating the efficacy of TNK compared to alteplase in acute AIS within 4.5 h from symptom onset showed no significant difference between these two agents with regard to functional outcome at 90 days but improved median time to treatment and large vessel recanalization in TNK-treated patients. The results from ongoing TNK trials in larger patient cohorts and in wake-up stroke populations will be instrumental to the wide-scale utilization of TNK in acute AIS management.

Purpose of review: To examine the emerging data for novel strategies being studied to improve use and dose titration of guideline-directed medical therapy (GDMT) for patients with heart failure (HF).

Recent findings: There is mounting evidence to employ novel multi-pronged strategies to address HF implementation gaps.

Summary: Despite high-level randomized evidence and clear national society recommendations, a large gap persists in use and dose titration of guideline-directed medical therapy (GDMT) in patients with heart failure (HF). Accelerating the safe implementation of GDMT has proven to reduce the morbidity and mortality associated with HF but remains an ongoing challenge for patients, clinicians, and health systems. In this review, we examine the emerging data for novel strategies to improve the use of GDMT including the use of multidisciplinary team-based approaches, nontraditional patient encounters, patient messaging/engagement, remote patient monitoring, and electronic health record (EHR)-based clinical alerts. While societal guidelines and implementation studies have focused on heart failure with reduced ejection fraction (HFrEF), expanding indications and evidence for the use of sodium glucose cotransporter2 (SGLT2i) will necessitate implementation efforts across the LVEF spectrum.

Purpose of review: To describe the role of iron deficiency in both heart failure and pulmonary hypertension.

Recent findings: To role of iron deficiency in heart failure is well established and pathophysiologic overlap with pulmonary hypertension exists.

Summary: Iron deficiency is common co-morbidity in heart failure and pulmonary hypertension. The high prevalence is intertwined into the pathophysiology of these conditions (e.g., neurohormonal activation, inflammation). The presence of iron deficiency has a negative impact on cardiomyocytes and cardiac function, skeletal muscle function, and pulmonary vascular function. In heart failure data from over 2000 randomized patients with iron deficiency using a uniform diagnosis, have illustrated beneficial effects on functional status, quality of life, reverse cardiac remodeling, and heart failure admissions. While iron deficiency is recognized to be prevalent in pulmonary hypertension and associated with worse functional status, the absence of a uniform definition and the absence of large prospective randomized controlled trials with iron therapies limits the conclusions on the causal role of iron deficiency such as observed in heart failure.

Purpose of review: The purpose of this review is to explore the prevalence and risk factors for a malignant phenotype in mitral valve prolapse (MVP) characterized by life-threatening ventricular arrhythmias and sudden cardiac arrest and death (SCD), including mechanistic and pathophysiologic findings and mechanism-based potential therapies.

Recent findings: A malignant phenotype in MVP characterized by life-threatening arrhythmias has long been recognized, although MVP is often benign. Efforts to identify this malignant phenotype have revealed potential risk factors for SCD that include elongated, myxomatous leaflets, ECG changes and complex ventricular ectopy. More recently, malignant MVP has been associated with myocardial fibrosis in the papillary muscles and inferobasal left ventricular wall. This localization suggests a central role of prolapse-induced mechanical forces on the myocardium in creating an arrhythmogenic substrate and triggering life-threatening arrhythmias. This mechanism for fibrosis is also consistent with imaging evidence of prolapse-induced mechanical changes in the papillary muscles and inferobasal left ventricular wall. Currently, no therapy to prevent SCD in malignant MVP has been established and limited clinical data are available. Mechanistic information and prospective study have the potential to identify patients at risk of SCD and preventive strategies.

Summary: Malignant MVP relates to unique properties and mechanical abnormalities in the mitral valve apparatus and adjacent myocardium. Increased understanding of disease mechanisms and determinants of arrhythmias is needed to establish effective therapies.