variety of aetiologies ranging from coronary artery disease, infections/myocarditis, toxins (alcohol and other drugs), metabolic or endocrine abnormalities, autoimmune disorders, infiltrative processes and a variety of genetic/inheritable disorders. In many cases, a distinct cause of the compromised heart muscle is never found. DCM can be asymptomatic, or it can result in symptoms of exercise intolerance, shortness of breath, swelling, congestive heart failure or SCD from ventricular arrhythmia. Prevalence The exact prevalence of DCM in the general population is not known and estimates depend on the population demographics and the cut-off used to define LV dysfunction.55 The majority of cases with early stages of LV dysfunction may be asymptomatic. 56 age, male gender and the presence of cardiovascular risk factors. Among a relatively young, healthy population without coronary risk factors, asymptomatic LV dysfunction was present in about 0.2% of individuals.57 Contribution as a cause of SCD DCM is associated with an increased risk of ventricular arrhythmias and sudden cardiac arrest, with highest risk seen among individuals with severe LV dysfunction. Notably, SCD can occur even in the absence of heart failure symptoms. In the Framingham Heart Study, the death rate from asymptomatic LV dysfunction was 6.5% per 100 personyears, with 53% of deaths occurring prior to the onset of symptoms, emphasising the importance of screening for this disorder.58 DCM accounts for about 2% of cases in a series of young athletes with sudden cardiac arrest.2 Diagnostic criteria DCM is diagnosed on non-invasive imaging (echocardiography or cardiac MRI) by detecting LV chamber enlargement and decreased LV systolic (contractile) function. Systolic function is usually quantified using either fractional shortening (FS) or ejection fraction (EF), but there is no consensus cut-off definition of DCM based on these parameters. Normal ranges vary by lab and imaging modality. Abnormal ECG findings in DCM Several studies have examined ECG abnormalities in patients with symptomatic DCM, but few have reported findings among non-ischaemic DCM or among individuals with asymptomatic LV dysfunction.59–61 Overall, approximately 90% of individuals with DCM have abnormal ECG finDCM prevalence is increased with older dings (figures 14 and 15). Patients with prior myocardial infarction may manifest pathological Q waves. Among individuals with non-ischaemic cardiomyopathy, the most common abnormalities seen include voltage criteria for LVH (33–40%), TWIs (25–45%), LAE (15–33%), LAD (15–25%), pathological Q waves (10–25%), LBBB (9–25%), premature ventricular contractions (5–10%) and RBBB (4%).62 These findings are non-specific for DCM. Goldberger has proposed a triad of findings that may offer more specificity: (1) LVH in the anterior precordial leads; (2) low limb lead voltage and (3) poor precordial R wave progression.63 Given the overlap of some of these findings with physiological ECG changes found in athlete’s heart, distinctly abnormal ECG criteria unrelated to regular training and requiring additioFigure 14. ECG from a patient with idiopathic dilated cardiomyopathy. Note the resting sinus tachycardia, left atrial enlargement, T wave inversions in the lateral limb (I and aVL) and precordial (V5–V6) leads and deep S waves in V1–V3 ( part of Goldberger’s triad). Figure 15. ECG of a young patient with dilated cardiomyopathy. Note inferior Q waves (II, III and aVF), poor R wave progression across the precordial leads with deep S waves in V1–V3, and a single premature ventricular complex. High-degree AV block is also present. nummer 4 | september 2013 | Sport & Geneeskunde 33 Pagina 32
Pagina 34Scoor meer met een online shop in uw magazines. Velen gingen u voor en publiceerden tijdschriften online.
Sport & Geneeskunde nummer 4 | September 2013 Lees publicatie 25Home