Background: Migraine is a prevalent episodic brain disorder known for recurrent attacks of unilateral headaches, accompanied by complaints of photophobia, phonophobia, nausea, and vomiting. Two main categories of migraine are migraine with aura (MA) and migraine without aura (MO). Main body: Early twin and population studies have shown a genetic basis for these disorders, and efforts have been invested since to discern the genes involved. Many techniques, including candidate-gene association studies, loci linkage studies, genome-wide association, and transcription studies, have been used for this goal. As a result, several genes were pinned with concurrent and conflicting data among studies. It is important to understand the evolution of techniques and their findings. Conclusions: This review provides a chronological understanding of the different techniques used from the dawn of migraine genetic investigations and the genes linked with the migraine subtypes.

The COVID-19 pandemic has had a profound global impact, with vaccination emerging as a key strategy for controlling the virus. However, concerns have arisen regarding potential cardiovascular side effects, particularly myocarditis following mRNA COVID-19 vaccination. This review examines the risk of post-vaccination myocarditis by analyzing over 40 studies. Findings indicate that myocarditis occurs most commonly within 2 to 4 days after the second dose, particularly in males aged 12 to 39 years. Proposed mechanisms include molecular mimicry and hypersensitivity reactions. Despite these concerns, most cases present with mild symptoms such as chest pain and dyspnea, resolving with supportive care. Importantly, the overall safety profile of COVID-19 vaccines remains high, with benefits significantly outweighing risks. Further multi-center studies are needed to fully understand the pathophysiology and mitigate potential adverse effects. No clinical trials were conducted for this review.

Background: Left ventricular (LV) mass and left atrial (LA) strain are physiologically coupled and individually predict adverse cardiovascular outcomes. Their imbalance may reflect early atrioventricular uncoupling and atrial myopathy before overt structural disease. Aims: We evaluated whether a cardiac magnetic resonance (CMR)-derived LV mass-to-LA strain ratio identifies early atrioventricular mechanical uncoupling and predicts cardiovascular events. Methods: Participants from the Multi-Ethnic Study of Atherosclerosis (MESA) underwent CMR at Exams 1 (2000–2002) and 5 (2010–2012). The LV mass-to-LA strain ratio was calculated as indexed end-diastolic LV mass divided by peak LA strain. Classification and regression tree analysis identified cut points for baseline ratio and longitudinal change, defining low (3.26) groups, and lesser-(≤130%) versus greater-change (>130%) groups. Multivariable Cox models assessed associations with heart failure (HF), atrial fibrillation (AF), myocardial infarction (MI), and all-cause mortality. Results: Among 4,232 participants (mean age 61.5±10.1 years; 52.8% female), the mean ratio was 1.95±0.72. Over a median 18-year follow-up, 6.0% developed HF, 5.2% MI, 18.7% AF, and 25.6% died. A high LV mass-to-LA strain ratio independently predicted HF (HR 2.85), AF (HR 2.00), MI (HR 1.96), and death (HR 1.70; all P≤.003). With repeat CMR, an increasing ratio also predicted cardiovascular events, including among individuals with normal LV mass and LA strain. Higher baseline ratios were associated with progression toward abnormal volumetric atrioventricular coupling over time. Conclusion: A higher LV mass-to-LA strain ratio and its increase independently predict cardiovascular events before overt chamber abnormalities, supporting impaired atrial adaptation as an early stage of atrial myopathy.

Aims: T1 mapping and extracellular volume (ECV) fraction are validated markers of diffuse myocardial fibrosis on cardiac magnetic resonance (CMR). Factors promoting left ventricular (LV) fibrosis are also linked to incident atrial fibrillation (AF), but whether ECV expansion is associated with increased AF risk remains unknown. Objectives: We evaluated whether baseline LV-ECV independently predicts incident AF. Methods and results: We studied 1261 participants from the multiethnic study of atherosclerosis (MESA) free of AF at baseline who underwent myocardial T1 mapping between 2010 and 2012. Participants were followed prospectively for incident AF. Associations between ECV and incident AF were assessed using multivariable Cox models adjusted for CHARGE-AF risk factors, with additional analyses adjusting for myocardial scar, left atrial (LA) structure and function, and LV ejection fraction (LVEF). During a median follow-up of 7.82 years, 156 participants developed AF. ECV was independently associated with incident AF after adjustment for CHARGE-AF risk factors (hazard ratios (HR) 1.105 per 1% increase; 95% CI 1.045–1.168; P < 0.001). Participants in the highest ECV quartile (>28.6%) had approximately a two-fold higher risk of AF compared with the lowest quartile (HR 1.914; 95% CI 1.198–3.058; P = 0.007). Associations remained significant after adjusting for myocardial scar, LA parameters and LVEF. Higher ECV was associated with adverse LA remodelling, including increased LA volume and impaired atrial emptying (P < 0.05), and remained associated with AF after LA adjustment. Conclusion: Diffuse LV interstitial fibrosis quantified by ECV independently predicts incident AF and is associated with adverse atrial remodelling, supporting ventricular fibrosis as an early substrate for AF development.