Mitral valve prolapse (MVP) is a relatively common mitral valvulopathy and the most common cause of isolated primary mitral regurgitation (MR) requiring surgical repair. It affects about 1–3% of the general population. Although MVP is viewed as a benign condition, the association between MVP and sudden cardiac death (SCD) has been proven. Patients with MVP have a three times higher risk of SCD than the general population. The underlying mechanisms and predictors of arrhythmias, which occur in patients with MVP, are still poorly understood. However, some echocardiographic features such as mitral annulus disjunction (MAD), bileaflet MVP (biMVP), and papillary muscle (PM) fibrosis were frequently linked with increased number of arrhythmic events and are referred to as “arrhythmogenic” or “malignant”. Arrhythmogenic MVP (AMVP) has also been associated with other factors such as female sex, polymorphic premature ventricular contraction (PVC), abnormalities of T-waves, and Pickelhaube sign on tissue Doppler tracing of the lateral part of the mitral annulus. Cardiac magnetic resonance (CMR) imaging and speckle tracking echocardiography are new tools showing significant potential for detection of malignant features of AMVP. This paper presents various data coming from electrocardiography (ECG) analysis, echocardiography, and other imaging techniques as well as compilation of the recent studies on the subject of MVP.

The use of echocardiography, a straightforward and widely available technique, allows for a comprehensive assessment of the patient with hypertrophic cardiomyopathy (HCM) under both resting and stress conditions. The true prevalence of HCM has been redefined over time by this imaging approach, which has also made it feasible to pinpoint parameters that clinicians may use to stratify patients at risk for adverse cardiovascular events. The current and emerging prognostic predictors in HCM, assessed with transthoracic echocardiography at rest and during provocation, are discussed in this review.

Coronary vasospasm stands as a widely acknowledged and frequent culprit behind chest pain, acute coronary syndrome, and sudden cardiac death, yet it remains a challenging diagnosis. Current guidelines recommend invasive coronary function testing to assess pathophysiology and mechanisms and to define treatment. In reality, this protocol is rarely applied, because it necessitates extended occupation of the cath lab, repetitive administration of nephrotoxic iodine contrast agents, the need for repeated testing on both coronary arteries leading to considerable radiation exposure, and significant direct expenses. The promising perspective for vasospasm testing is a noninvasive approach with advanced echocardiographic techniques, such as transthoracic Doppler echocardiography, with more sensitive indicators of ischemia. Hyperventilation and exercise tests are used for vasospasm directed testing, with assessment of the new parameters: coronary flow velocities and reserve, allowing to see deeper into macro and microvascular pathophysiology. Association between coronary flow, global longitudinal strain and microvascular dysfunction (MVD) and impaired values at hyperemia was previously demonstrated. Reduction in coronary flow velocity (CFV) despite heightened myocardial oxygen consumption and double product during hyperventilation are indicative of coronary vasospasm. Normal coronary angiography finding in patients with documented evidence of ischemia should initiate additional diagnostic testing in order to increase the yield of specific diagnosis in patients with suspected vasospasm, which could help to personalize treatment and prognosis. In order to achieve this, non-invasive provocative stress echocardiography tests should be included in the diagnostic workup. This approach, characterized by its simplicity, feasibility, safety, and efficacy, is currently undergoing extensive testing on a large scale.

Lipoprotein(a) [Lp(a)] is composed of a low-density lipoprotein (LDL) and glycoprotein (a)—apolipoprotein(a) [apo(a)]. The size and concentration of Lp(a) in serum can vary among individuals and is determined by genetic factors. The environmental factors, diet, and physical activity have a negligible effect on Lp(a) level. Observational, epidemiological, and genetic studies improved that high levels of Lp(a) > 50 mg/dL (> 125 nmol/L) have been associated with an increased risk of myocardial infarction (MI), stroke, and calcific aortic valve stenosis (CAVS). It is recommended to measure Lp(a) at least once in adults to identify individuals with a high cardiovascular risk. This screening is particularly important in certain populations, including: youth with a history of ischemic stroke or a family history of premature atherosclerotic cardiovascular disease (CVD; ASCVD) or high Lp(a), individuals with recurrent cardiovascular events despite optimal hypolipemic treatment and no other identifiable risk factors or patients with familial hypercholesterolemia (FH). Considering Lp(a) levels in the evaluation of cardiovascular risk can provide valuable information for risk stratification and management decisions. However, it’s important to note that the treatments of elevated level of Lp(a) are limited. In recent years, there has been ongoing research and development of new drugs targeting Lp(a): pelacarsen—antisense oligonucleotide (ASO), and olpasiran—a small interfering RNA (siRNA).

Alcohol drinks, especially wine, have been described since 6,000 B.C. For many years in modern medicine, wine in moderation has been considered healthy for cardiovascular prevention, i.e., recommended by nutrition committees. Some regional guidelines still recommend one to two standard drinks per day. By the very recent (January 2023), World Health Organization and Canadian Guidance on alcohol emphasize that any alcoholic drink is hazardous to the health and the safe amount is zero. The risk starts with every single drop. It was also nicely summarized in the manuscript “Alcohol-dose question and the weakest link in a chemical interplay” (Explor Cardiol. 2023;1:15–25. doi: 10.37349/ec.2023.00003) especially from the standpoint of a researcher in the cardiovascular arena. The newest recommendations are based on observational studies and their meta-analysis, therefore establishing associations, pointing out that alcohol may somewhat prevent cardiovascular diseases and diabetes type 2, but with a significant increase in non-cardiovascular morbidity and mortality, especially cancers. Previous recommendations, therefore, may be obsolete as they were based on studies where abstainers from alcoholic beverages had inherent higher risks. The current controversy with conflicting guidelines for alcoholic beverage consumption in the era of precision medicine may stimulate more fundamental investigations up to genetic ones and find the cause-effect relations. In the era of precision medicine, it may come closer to discovering the causes of cancers and many other diseases, enabling predictions of reactions to alcoholic beverages by each person, not just in the population.

Congenital heart defects (CHD) represent the most frequent congenital anomalies among newborns, as well as the leading cause of spontaneous abortion, stillbirth, neonatal and infant death. CHD have been recognized as multifactorial diseases, with environmental contaminants as potential contributors to the etiopathogenesis of CHD. Toxic elements, such as arsenic (As), cadmium (Cd), lead (Pb), and mercury (Hg) are known to be associated with adverse reproductive outcomes and certain congenital anomalies, however their association with the risk for CHD remains inconsistent. This review summarizes the updated evidence on the CHD-associated risk related to exposure to As, Cd, Hg, Pb during pregnancy, reporting the main findings from epidemiological and experimental studies and the underlying molecular mechanisms. Additionally, being diet the major source of these elements in the general population, after having identified the main vectors of toxic metals in food, possible remediation strategies to reduce diet-related risks are also described. Among these, a novel, consumer-centered approach in developing new foods is discussed, considering not only the nutritional characteristics of edible compounds foods are made up of, but also their organoleptic features, making the food even more appealing to the consumer. Overall, current data support the association of maternal exposure to As and Pb with increased risk for CHD, although significant associations have only been observed for total and/or specific subgroups. On the other hand, the evidence of association for Cd and Hg exposure in pregnancy with CHD in the offspring remains, yet, quite speculative. Further large prospective cohort studies and insights into the molecular and biomolecular processes of these relationships are warranted to further explore and/or verify these findings.