Acute pulmonary embolism (PE) is a leading cause of mortality. Not only is PE associated with short-term mortality, but up to ~20% of patients might suffer from long-term consequences such as post-PE syndrome and chronic thromboembolic pulmonary hypertension. Current risk stratification tools poorly predict those who are at risk for short-term deterioration and those who develop long-term consequences. Traditionally, systemic thrombolysis has been considered the first-line therapy for patients with high-risk PE without contraindications; however, it comes with the risk of major bleeding (notably intracranial hemorrhage). The use of catheter-directed interventions (embolectomy or thrombolysis) has been increasing owing to their low bleeding risk; however, randomized trial data supporting their efficacy in improving clinical outcomes are limited. In this review, we highlight the evidence supporting the available advanced therapies for high- and intermediate-risk PE and summarize the ongoing trials which are evaluating these therapies.

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.

Introduction and importance: Stress cardiomyopathy refers to a syndrome of acute but reversible left ventricular dysfunction, often triggered by emotional or physical stress. Reverse Takotsubo cardiomyopathy is an uncommon variant that occurs in about 5% of cases. Classically, it has been known to be following a catecholamine surge due to physical or emotional stress. This case highlights the importance for physicians to be aware of the possibility of developing stress cardiomyopathy in patients with acute intra-abdominal processes. Case presentation: Forty-one-year-old Caucasian female with was admitted with an acute small bowel obstruction. After failing conservative management, it was decided to proceed with surgery. After induction with anesthesia but prior to the surgeons first incision, the patient developed a tachyarrhythmia with hemodynamic compromise requiring the surgery to be aborted. That evening, she developed chest pain with concerns for an acute coronary syndrome. She was taken urgently to the for invasive angiography, which demonstrated reverse Takotsubo. Clinical discussion: Intra-abdominal processes and intubation have previously been reported be catalyst for this disease process. This patient had multiple stressors including mechanical bowel obstruction and anesthesia after failing conservative management. The diagnosis was confirmed by coronary angiography and left ventriculogram, and followed up with repeat outpatient echocardiography. Conclusion: A case of small bowel obstruction that developed reverse Takotsubo preceded by sustained ventricular tachycardia after intubation. The patient did well and had complete recovery cardiac function. Risk factors and underlining mechanism for the different variants of stress cardiomyopathy are not well understood, further investigation is warranted.

Seventy‐year‐old male with primary progressive multiple sclerosis that had a severe episode of oropharyngeal dysphagia following initiation of carbamazepine. He was being treated for trigeminal neuralgia. Four days after discontinuation of carbamazepine resulted in a complete resolution of the patient's dysphagia, and he returned to baseline.

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.