Transthoracic echocardiography (TTE) is a second-line, problem-solving study in myasthenia gravis (MG) used to characterize suspected cardiac involvement rather than to screen unselected patients.^[1] In a large Medicare cohort, cardiovascular disorders were the leading cause of death in MG patients with a cause-specific mortality proportion comparable to matched controls (15.3% vs 15.7%; all-cause mortality was higher in MG but non-significant after comorbidity adjustment), and functional imaging typically reveals only minor, subclinical dysfunction.^[2] Clinically overt cardiac involvement is rare, but a spectrum of disease exists—including subclinical diastolic dysfunction, myocarditis, dilated and Takotsubo cardiomyopathy, and reduced ejection fraction—that carries prognostic significance and requires targeted management.^[1][3]

• TTE is indicated when clinical features (unexplained fatigue, dyspnea, heart failure signs), ECG abnormalities, or elevated cardiac biomarkers (troponin, BNP/NT-proBNP) raise concern for myocarditis, cardiomyopathy, or heart failure.^[3]
• Routine echocardiographic screening in asymptomatic MG patients is not recommended.^[1][3]
• In a cohort of MG patients without pre-existing cardiovascular disease, an abnormal ECG predicted echocardiographic cardiac damage (ejection fraction <55% or E/e′ >8) with high discrimination, whereas systolic impairment was observed exclusively in patients with ECG abnormalities—supporting an ECG-first diagnostic pathway.^[3]

• Diastolic Dysfunction: The most consistently reported echocardiographic abnormality. Features include reduced peak filling rate, reduced E velocity, increased A velocity, and a reduced E/A ratio with preserved ejection fraction (EF). Mean E/e′ is mildly elevated (10.5 ± 3.2), with significantly higher ratios observed in patients with baseline ECG abnormalities.^[4][3]
• Systolic Dysfunction: Left ventricular ejection fraction (LVEF) <55% is uncommon; when present, it carries a worse prognosis but may improve with immunosuppressive therapy.^[3]
• Deformation Imaging: Global longitudinal strain (GLS) and tissue Doppler imaging demonstrate higher sensitivity than standard LVEF for detecting subtle myocardial injury. In ICI-related myocarditis, reduced GLS predicts major adverse cardiovascular events (MACE) even in patients with preserved LVEF; each 1% absolute reduction in GLS was associated with an approximately 4-fold increase in major adverse cardiovascular events among patients with preserved LVEF.^[5][6]

• Reported in up to 10% of MG cohorts in specialized series, primarily associated with thymoma-associated MG and autoantibodies against cardiac antigens (anti-Kv1.4, anti-titin, and anti-ryanodine receptor).^[7]
• TTE findings include regional wall motion abnormalities, global systolic dysfunction, or isolated diastolic dysfunction.^[8]
• A normal TTE does not exclude early or localized myocarditis; cardiac MRI using the modified Lake Louise criteria (T1/T2 mapping, late gadolinium enhancement) is the reference imaging modality. In ICI-associated myocarditis, late gadolinium enhancement is present in approximately 48% and T2 signal elevation in 28% of confirmed cases; therefore, CMR sensitivity is imperfect, and a negative CMR does not exclude myocarditis, particularly early in its course.^{[8][6][9][10]}

• A recognized complication of myasthenic crisis, characterized by transient left ventricular apical ballooning with basal hyperkinesis extending beyond a single coronary distribution.^[11][12]
• LV dysfunction resolves spontaneously on serial echocardiography over days to weeks in most surviving cases.^[13][14]

• In patients receiving immune checkpoint inhibitors (e.g., anti-PD-1/PD-L1 agents), MG or MG-like syndrome can co-occur with myositis and myocarditis (the “3M” overlap syndrome).^[9][15]
• Reduced left ventricular ejection fraction is present in roughly one-third to one-half of ICI myocarditis cases, with the majority—and most fatal cases—showing preserved LVEF; conduction disturbances dominate and are the leading cause of death in fatal presentations. A normal LVEF therefore does not rule out life-threatening myocarditis.^[16][6][15]

Historical Doppler studies noted acute changes in LV diastolic filling parameters following acetylcholinesterase inhibitor administration.^[4] Subsequent tissue Doppler evaluation confirmed lower early-diastolic annular velocity and strain prior to pyridostigmine dosing that normalized post-administration, with no persistent conventional echocardiographic abnormalities after adjusting for blood pressure.^[17] These observations reflect acute autonomic and loading alterations rather than reversible structural cardiomyopathy and do not justify serial echocardiographic monitoring.^[17]