Hypertrophic cardiomyopathy (HCM) is often associated with left ventricular outflow tract (LVOT) obstruction, which affects a substantial proportion of patients. This obstruction results from a range of anatomical abnormalities involving both the valvular and subvalvular structures. Pharmacological therapies play a pivotal role in the management of LVOT obstruction, with a range of drug classes exhibiting distinct mechanisms of action. Beta-blockers, including atenolol and nadolol, are considered the first-line treatment due to their ability to reduce heart rate and myocardial contractility and enhance diastolic filling. Non-dihydropyridine calcium channel blockers, such as verapamil and diltiazem, are utilized as second-line agents when beta-blockers are ineffective or contraindicated. Disopyramid, a Class 1A antiarrhythmic agent, is employed for patients who do not respond to initial therapeutic interventions and can reduce LVOT gradients. Recent advancements in cardiac myosin modulators, such as Mavacamten and Aficamten, offer targeted therapies by modulating myosin–actin interactions to reduce LVOT gradients and improve symptoms, with promising results from clinical trials. Although gene therapy is still in its nascent stages, it has the potential to address the genetic basis of HCM by employing techniques such as genome editing, gene replacement, and the modulation of signaling pathways. For patients exhibiting severe symptoms or demonstrating unresponsiveness to medical treatment, invasive therapies, such as septal reduction therapy and alcohol septal ablation, are considered. Ultimately, the treatment and prevention of atrial fibrillation and sudden cardiac death are two key points of HCM management in both obstructive and non-obstructive forms. This review aims to provide an overview of current pharmacological and invasive strategies, as well as emerging therapies, in the management of HCM.

At its earliest appearance, atrial fibrillation (AF) is often unnoticed, asymptomatic, and/or merely device-detected. Widespread use of heart-rate monitoring technologies has facilitated such “nascent atrial fibrillation (nAF)” recognition. Consequently, clinicians face a growing number of patients affected by new-onset AF in the absence of a definite indication for anticoagulation due to several counterarguments: (1) a CHA₂DS₂-VA score ≤ 1 in otherwise apparently healthy subjects; (2) an uncertain embolic/hemorrhagic benefit/risk ratio with anticoagulation; (3) EKG demonstration and confirmation of AF; and (4) existence of a pathogenic mechanism other than atrial hypercoagulability. In this frustrating limitation of pharmacological options, cardiologists may miss a complete comprehension of drugs with proven anti-ictal potential, whose administration may serve both as a bridge strategy toward future anticoagulation and as a consolidative strategy paralleling anticoagulation. This review aims to summarize and elucidate such therapeutic strategies and their preventative mechanisms.

Mitral annular disjunction is related to increased arrhythmogenic risk; in a certain percentage of cases, mitral annular disjunction is associated with tricuspid annular disjunction. While the prognostic implications of mitral annular disjunction have been well established, there is still little data to define this aspect regarding the tricuspid annular disjunction. We present a case of a patient admitted for life-threatening ventricular arrhythmias that occurred during endurance sporting activity, who was found to have isolated tricuspid annular disjunction, not associated with mitral annular disjunction. Based on several factors, including the morphology and axis of QRS of the ventricular arrhythmic activity, and its behavior, including the response to antiarrhythmic treatment, and in keeping with the finding of edema and late gadolinium enhancement at the basal segment of the right ventricle free wall on cardiac magnetic resonance imaging, a direct relation between tricuspid annular disjunction and ventricular arrhythmias was highly conceivable. Control after three months showed almost complete remission of the previously described and persistence of LGE at the level of the basal segment of the free wall of the right ventricle, so giving strength to the hypothesis of an event related to increased acute RV free wall stress, secondary to high-intensity physical activity, established on a framework of chronic wall stress, as represented by LGE, similarly to what happens for mitral valve prolapse. To the best of our knowledge, this is the first case of a legitimately conceivable direct relation between tricuspid annular disjunction and ventricular arrhythmias.

Hypertrophic cardiomyopathy (HCM) is a cardiac disorder characterized by unexplained left ventricular hypertrophy and a clinical presentation that is heterogeneous, ranging from asymptomatic cases to sudden cardiac death (SCD). The condition’s complex pathophysiology encompasses myocyte disarray, fibrosis, and impaired cellular metabolism. Advancements in non-invasive cardiac imaging, notably echocardiography and cardiac magnetic resonance (CMR), have led to substantial progress in the domains of early diagnosis, phenotypic characterization, and risk stratification. Echocardiography is the preferred diagnostic modality, as it provides a comprehensive evaluation of ventricular hypertrophy patterns, left ventricular outflow tract (LVOT) obstruction, mitral valve abnormalities, left atrial size, and diastolic function. Novel techniques, such as speckle-tracking strain imaging, have emerged as means to detect subclinical myocardial dysfunction and to provide significant prognostic information. Cine-CMR sequences, tissue characterization with late gadolinium enhancement, and quantitative techniques such as strain imaging have been shown to enhance diagnostic precision and prognostic evaluation. The integration of multimodality imaging has been demonstrated to enhance the management of patients with HCM, both in the short term and in the long term, by facilitating individualized monitoring. This review summarizes the role of cardiac imaging in the comprehensive evaluation of HCM, emphasizing the impact of these methods on diagnosis, risk assessment, and personalized patient care, particularly in challenging clinical settings, such as cases of athlete’s heart and pathological ventricular hypertrophy.

COVID-19 and sepsis pose great challenges to clinicians and growing evidence is demonstrating links between the two conditions. Both can be complicated by acute heart failure. The use of levosimendan in patients with ventricular dysfunction during COVID-19 infection and sepsis has very little evidence. A 46-year-old, hypertensive and obese patient was admitted for severe left ventricular failure and shock during sepsis following a COVID-19 infection. The patient was treated first with norepinephrine, which was partially effective, then with the addition of levosimendan as a continuous 24 hours infusion. Vital signs and echocardiographic systolic performance indices, such as FE, SVi, CI, dP/dT, TAPSE, and tricuspid S-wave velocity, as well as diastolic function, were recorded at access, 12 and 24 hours. After initiation of levosimendan, a rapid improvement in vital signs and systolic and diastolic performance indices was observed, not depending on changes in preload, afterload, and inflammatory status. Blood cultures were negative for the presence of bacteria, thus defining the picture of likely viral sepsis. Cardiac magnetic resonance was determinant, showing a picture of myocarditis sustained by immune processes rather than direct viral injury, which was confirmed by endomyocardial biopsy. In conclusion, this case highlights the efficacy of levosimendan in acute heart failure complicated by shock due to COVID-19-related myocarditis and concomitant sepsis and confirms cardiac magnetic resonance as the gold standard for the diagnosis of myocardial inflammatory disease. To the best of our knowledge, this is the first documented case of effective use of levosimendan in this context.