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.

Left-ventricular non-compaction (LVNC) is a recently classified cardiomyopathy that involves abnormal trabeculations inside the left ventricle, most commonly located in the ventricular apex. There are 9 distinct types of non-compaction cardiomyopathy that can impact both the left and right ventricles with subtypes involving mostly pediatric patients with concurrent congenital heart disease (CHD), to individuals in late adult-staged ages. LVNC affects the population with an estimated range of incidence from 0.014% to 1.3% and the disease can be diagnosed with the utilization of imaging studies such as transthoracic echocardiography (TTE). LVNC can also impact and lead patients to develop heart failure with estimated prevalence that can reach to 3–4% during their lifetime. LVNC often leads to complications such as heart failure, arrhythmias, and thromboembolic events and without adequate medical management and pharmacological therapies this can progress and lead to worsening cardiac function, sudden cardiac arrest, and even death. There are no strict guidelines organized for screening and monitoring for LVNC in patients except with the inclusion of having a high suspicion in patients without other cardiac abnormalities. Thus, more advanced clinical research and the establishment of diagnostic protocols needs to be standardized in order to further investigate the causes, prognostic factors and therapeutic modalities of patients with LVNC. The field of LVNC cardiomyopathy is expanding but better understanding of the pathophysiology and genetic influence of this cardiac disease is vital for the precision treatment and personalized care of LVNC.