Infective endocarditis (IE) is an infection of the endocardial surface of the heart involving native or prosthetic valves, endocardial structures, or intracardiac devices/leads. Unfortunately, incidence has risen in many settings over recent years. Historically, the incidence has been about 3–10 cases for every 100,000 person-years and was elevated to about 13.8 cases per 100,000 person-years in 2019. Despite advancements in both detection and treatment, mortality remains high, seen with inpatient mortality rates of 18%, along with a 6-month mortality rate of 30%. IE can be a fatal condition if left untreated, in part due to the multiple serious complications that can arise. By anticipating certain complications, clinicians can be better prepared to treat patients with this condition. This article provides an integrative review of the potential complications of IE. These complications vary depending on whether the patient has native or prosthetic valves. There are cardiac, embolic, and immune-complex mediated complications that can occur. Ultimately, IE can lead to multiorgan dysfunction and result in septic shock and disseminated intravascular coagulopathy (DIC). While the mainstay of treatment for IE remains medical, certain cases require surgical intervention. Due to their close relationship, a review of the indications for surgery in the treatment of IE is also presented in this article. By having a general scope of the complications of IE and when to get a surgical consult, clinicians can be better equipped to care for patients with a potentially fatal condition that is becoming increasingly more frequent.

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.