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EDMD classically presents with muscle weakness, early contractures, cardiac conduction abnormalities and cardiomyopathy, although the presence and severity of these manifestations vary by subtype and individual. Associated genes include <jats:italic>EMD<\/jats:italic>, <jats:italic>LMNA<\/jats:italic>, <jats:italic>SYNE1<\/jats:italic>, <jats:italic>SYNE2<\/jats:italic>, <jats:italic>FHL1<\/jats:italic>, <jats:italic>TMEM43<\/jats:italic>, <jats:italic>SUN1<\/jats:italic>, <jats:italic>SUN2<\/jats:italic>, and <jats:italic>TTN<\/jats:italic>, encoding emerin, lamin A\/C, nesprin\u20101, nesprin\u20102, FHL1, LUMA, SUN1, SUN2, and titin, respectively. The Online Mendelian Inheritance in Man database recognizes subtypes 1 through 7, which captures most but not all of the associated genes. Genetic diagnosis is essential whenever available, but traditional diagnostic tools can help steer the evaluation toward EDMD and assist with interpretation of equivocal genetic test results. Management is primarily supportive, but it is important to monitor patients closely, especially for potential cardiac complications. 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