Indian Journal of Clinical Cardiology

Extensive research on Lipoprotein(a) (Lp(a)) levels and their link to morbidity and mortality in regard to cardiovascular risk remains a cornerstone of cardiovascular studies. Recent findings suggest that in younger patients, Lp(a) serves as an independent risk factor for cardiovascular diseases (CVD). This is mediated by diverse processes, including signaling processes driving angiogenesis, cellular Inflammation and proliferation, cytokine formation, and antifibrinolytic activity. In addition, Lp(a) mediates the atherogenic properties of low-density lipoprotein (LDL).

Studies have shown worse long-term CVD morbidity and mortality outcomes, including acute myocardial infarction (MI), coronary atherosclerosis, and stroke in individuals with elevated plasma Lp(a) concentrations. In recent times, studies have also suggested a link between Lp(a) levels and calcified aortic valve disease (CAVDs), indicating that higher Lp(a) levels are associated with a faster progression of aortic stenotic valvular disease. In this review article, we discussed the effects of lifestyle modification, such as nutrition and exercise, on Lp(a) concentration, with a recommendation to promote novel therapeutic approaches to reducing Lp(a) levels. Given the significance of predicting atherosclerotic cardiovascular disease (ASCVD) risk through Lp(a) measurement, its importance cannot be overstated.

The Lp(a) lowering effect of proprotein convertase subtilisin/kexin type 9 (PCSK9) mAbs and lipoprotein apheresis has been well established. In contrast, the effects of statins, fibrates, ezetimibe, niacin, and bempedoic acid on Lp(a) levels have been inconsistent. New emerging therapies with significant promise target RNA molecules to modify protein production and lower Lp(a). Further research is required to facilitate modalities to explore Lp(a) further and tackle cardiovascular morbidity and mortality.

Ivabradine, a medication that selectively lowers heart rate by inhibiting the funny current (If) in the sinus node, has shown significant potential in managing various cardiac conditions. It has unique properties as a hyperpolarization-activated cyclic nucleotide-gated (HCN) channel blocker, primarily used in cardiology and cardiovascular medicine. It is primarily employed to lower heart rate in chronic stable angina, heart failure, and inappropriate sinus tachycardia. Ivabradine’s unique mechanism selectively reduces heart rate without affecting contractility or blood pressure, making it valuable, especially for patients who cannot tolerate β-blockers due to comorbidities. Indeed, it effectively reduces the occurrence of angina attacks and the need for short-acting nitrates, maintaining its anti-anginal benefits over the long term. This review provides insights into Ivabradine’s molecular mechanism, efficacy, clinical manifestation, and potential future applications in managing various cardiovascular conditions.

Cardiovascular diseases continue to be the leading cause of mortality and morbidity in the world. The prevalence has been changing with time in the developing and developed world. The higher prevalence in the South Asian population compared to the rest of the world has been reviewed with multiple theories, ranging from genetic predisposition, higher prevalence of diabetes mellitus, dietary patterns, and dyslipidemia with low high-density lipoprotein. The traditional risk scores are still underestimating cardiovascular risk in the large young population of the Indian subcontinent. There is a need to risk-stratify at an early age to start preventive measures early to save lives. The development of risk scores like Framingham Risk Score, QRISK, and ASCVD has been reclassified by adding the CT coronary calcium score. Further enhancing the risk by adding polygenic risk score for coronary artery disease and cardiometabolic disorders will guide us to start preventive measures early in life.

Recent advancements in intravascular imaging technologies have transformed our capacity to precisely identify and assess the culprit lesions responsible for acute coronary syndrome in clinical practice. Acute coronary syndrome commonly results from atherosclerotic plaque rupture, causing intracoronary thrombosis and acute myocardial ischemia, frequently presenting with chest discomfort and dyspnea. Intravascular imaging techniques, including near-infrared spectroscopy, optical coherence tomography, and intravascular ultrasound, provide more detailed insights into high-risk coronary lesions, overcoming the limitations of traditional coronary angiography. There is a growing clinical interest in the use of in vivo intravascular imaging to precisely characterize the morphology of atherosclerotic plaques, which are influenced by local hemodynamic flow. This article aims to offer a thorough examination of intravascular imaging technologies and physiological assessments, emphasizing their clinical utility in diagnosing and managing acute coronary syndrome, while also exploring their potential in shaping personalized treatment strategies to enhance patient outcomes.

Kounis syndrome is a rare phenomenon wherein cardiovascular symptoms develop after allergic or hypersensitivity reactions. We present the case of a 51-year-old male who developed anaphylactic shock after consuming kiwi fruit juice, followed by acute ST-elevation myocardial infarction (STEMI). Coronary angiography showed normal coronary arteries. This case emphasizes the importance of considering Kounis syndrome in patients with anaphylaxis and acute coronary symptoms.

Ventricular septal rupture is a rare mechanical complication of acute myocardial infarction that continues to have high mortality outcomes in the 21st century. Mechanical complications rarely co-occur after myocardial infarction, posing significant management challenges. We present an extremely rare case of a true ventricular double rupture in a patient with inferior wall myocardial infarction and its management implications, wherein the second rupture may be missed.

Persistently high-raised eosinophils are the hallmark of the rare heterogeneous group of illnesses known as idiopathic hypereosinophilic syndrome (HES). Eosinophil-mediated multiorgan damage is often the result of chronic illness. Although it can affect any organ, the heart, lungs, brain, spleen, and skin are frequently impacted. It may occasionally be necessary for management to use a multidisciplinary team approach. Cardiac involvement in the form of endomyocardial fibrosis or thromboembolic complications is frequent in the active disease. In HES, native and prosthetic mitral valve involvement is common; aortic valve involvement is extremely uncommon.

This case represents an unusual instance of prolonged aortic valve thrombosis in a male patient in his early fifties diagnosed with HES. Appropriate administration of blood-thinning agents and immunosuppressive treatment promotes effective management of thrombotic complications and associated symptoms, which eventually prevents further embolic problems and preserves the native valve.

Myocardial bridging of the coronary artery has been increasingly recognized as a cause of angina, myocardial ischemia, and sudden cardiac death owing to the advanced imaging systems being available. It has been most commonly found to occur in the left anterior descending artery as it runs down the interventricular groove between the right and left ventricle. Here we report two cases of isolated right coronary artery bridging with different clinical profiles and their importance in clinical practice. We also discuss the pathophysiology, complications, and management of myocardial bridging in regard to the two cases.

Chest pain from myocarditis may resemble typical angina and may be accompanied by ECG changes including ST segment elevation. Acute myocarditis is a known cause of ST elevation but there are no reported cases of acute myocarditis presenting as transient ST elevation in a specific coronary territory. We report the case of a young male who presented as STEMI but his coronary angiogram was normal and ST elevation settled down immediately after coronary angiography. Hence, a high index of suspicion in an appropriate clinical setting can avoid inadvertent coronary angiography or thrombolysis in these patients.

We report about a middle-aged male patient with rheumatic heart disease who had undergone an older generation tilting disc prosthetic aortic valve (Björk–Shiley valve) implantation 36 years back. He presented with severe mitral stenosis and a normal functioning prosthetic aortic valve. This case may be one of the longest reported functioning Björk–Shiley valve at aortic position, associated with an uneventful course over four decades. Patients with durable older generation prosthetic heart valves may be encountered in clinical practice and need to be managed in line with current guidelines.

A young adult in their 20s with recurrent presyncope, a diagnosed case of complete heart block, underwent a dual-chamber pacemaker implantation with left bundle branch area pacing (LBBAP). An immediate post-procedure electrocardiogram (ECG) showed atrial and ventricular paced complexes. However, an ECG two hours later showed no pacing pulses with an extremely prolonged PR interval of 400 ms. What is the probable mechanism?

This journal scan presents recent advances in pharmacotherapy, including obicetrapib, tirzepatide, plozasiran, and solbinsiran. It also discusses polymeric heart valves and demographic thresholds for hypertrophy in the diagnosis of obstructive hypertrophic cardiomyopathy. Additionally, we highlight important trials presented at the EURO PCR 2025, held in Paris, France.