Heart failure is a heterogeneous disorder that can lead to cardiogenic shock. Mechanical circulatory support (MCS) devices can replace the cardiac function in an attempt to bridge patients to transplant or they can serve as destination therapy to improve overall patient functionality and in turn quality of life. Currently utilized MCS devices include devices such as Left Ventricular Assist Devices (LVADs), Biventricular Assist Devices (BiVADs), Impella, Total Artificial Hearts (TAHs), and extracorporeal membrane oxygenation (ECMO). This literature review examines a range of studies, case reports, and meta-analyses to present current approaches to mechanical circulatory support (MCS), along with the challenges and limitations of existing devices, common complications, and overall survival and long-term outcomes following MCS therapy.

Calcified coronary lesions remain a challenge in percutaneous coronary intervention (PCI) in both situations of acute myocardial infarction (MI) and stable coronary syndrome. It significantly increases the risk of procedural complications due to difficulty in equipment delivery, balloon expansion, and stent delivery. Furthermore, stent thrombosis, dissection, perforation, and future in-stent restenosis occur more frequently in calcified coronary lesions, impacting repeat target vessel revascularization and increasing the risk of future MI. With intracoronary imaging (intravascular ultrasound and optical coherence tomography), peri-procedural success for treating calcified lesions has increased significantly. Different modalities of calcium modification techniques have since been introduced. This review will discuss the pathophysiology and phenotypes of calcium deposition in the coronary vessels, including eccentric calcified plaques and calcified nodules. We will also focus on calcium modification techniques and their mechanisms: (1) Balloon escalation technique, (2) intravascular lithotripsy, (3) orbital atherectomy, and (4) rotational atherectomy. We will focus on the strengths and limitations of each technique, based on current recommendations and expert consensus from SCAI. We will also provide contemporary evidence of each modality for treating different phenotypes of calcified lesions. In summary, this article provides a comprehensive review of current guidelines for optimizing the treatment of calcified coronary lesions in PCI.

Coronary microvascular dysfunction (CMD) is a prevalent and clinically important cause of myocardial ischemia across the spectrum of coronary artery disease, including patients with angina and nonobstructive coronary arteries, persistent symptoms after revascularization, and acute coronary syndromes. Despite its prognostic significance, CMD remains underrecognized due to the limitations of angiography-centered evaluation and the heterogeneity of underlying biological mechanisms. This review presents a physiology-based framework for the assessment of CMD, emphasizing the role of invasive coronary function testing in defining mechanistic endotypes and informing clinical interpretation. We summarize the biological foundations of CMD, including endothelial dysfunction, vascular smooth muscle hyperreactivity, structural remodeling of the microcirculation, and extravascular myocardial influences, and describe how these processes manifest as distinct but overlapping clinical phenotypes. Contemporary invasive physiologic tools—coronary flow reserve, index of microcirculatory resistance, and vasomotor testing with acetylcholine—are reviewed with a focus on their complementary roles in localizing disease within the coronary circulation. The clinical application of microvascular testing is discussed in both stable coronary syndromes and acute coronary syndromes, highlighting differences in diagnostic intent, prognostic implications, and therapeutic relevance. We distinguish chronic CMD in stable syndromes from post–myocardial infarction microvascular injury, in which invasive indices have primarily prognostic implications. By integrating coronary biology, invasive physiology, and clinical context, this review supports a shift from purely anatomic assessment toward a mechanism-based, physiology-driven approach to ischemic heart disease.

Heart transplantation (HT) remains a critical treatment for patients with end-stage heart failure who remain unresponsive to optimized guideline-directed medical therapy. This review examines recent advancements in pre-, peri-, and post-transplant screening and management aimed at improving patient selection, transplant accessibility, and clinical outcomes. Pre-transplant strategies include comprehensive HT candidate evaluation, risk stratification, donor selection, allocation policies that priotize critically ill patients, and mechanical circulatory support (MCS) to stabilize patients awaiting transplantation. Peri-transplant advances focus on strategies to maintain hemodynamic stability, minimize ischemic injury, and maintain graft viability immediately after HT. Post-transplant management emphasizes individualized immunosuppressive regimens, cardiac allograft rejection surveillance, and the prevention and management of complications to improve graft survival and long-term patient outcomes. Despite substantial progress, significant challenges remain, particularly the shortage of suitable donor organs and the risk of immune-mediated graft rejection. Emerging approaches, including artificial intelligence, xenotransplantation, and regenerative medicine, offer promising opportunities to expand the donor pool, enhance clinical decision-making, and improve HT outcomes. This review examines the research that influences the current policies and practices involved in HT, featuring the pivotal findings as well as any shortcomings present among these studies. Ultimately, continued research and multidisciplinary collaboration in each phase of HT are essential to improve the short and long-term health outcomes of transplant candidates. By integrating established evidence-based practices with emerging technologies, clinicians may further improve equitable access, survival, and quality-of-life for patients with end-stage heart failure.

Pulmonary hypertension (PH) can be defined as a mean pulmonary artery pressure (mPAP) greater than 20 mm Hg at rest during right heart catheterization (RHC). The reported prevalence of PH throughout the globe has been estimated to impact approximately 1% of the total population, with a majority of those afflicted being women more than men. Numerous etiologies give rise to the pathophysiology of PH, including heart disease (i.e., left-sided heart failure), lung diseases, and other unclear causes related to chronic stages and complications surrounding long-standing pulmonary thromboembolisms, side effects of certain medications, and genetic and environmental factors. Untreated PH can lead to severe morbidities such as cardio-renal syndrome and congestive hepatopathy (cardiac cirrhosis). Management of PH focuses on decreasing pulmonary pressures by using vasodilators such as prostanoids, and phosphodiesterase type 5 (PDE-5) inhibitors, as well as newer treatments such as sotatercept, which inhibits activin signaling, thereby inhibiting excessive cell growth in the pulmonary artery vasculature and down-regulating the pro-proliferative pathways.