هبوط الصمام التاجي في تخطيط القلب

كيف يظهر في التخطيط

There is no specific ECG pattern in mitral valve prolapse — the diagnosis is made echocardiographically. In most patients, the ECG is within normal limits; some reveal concomitant electrophysiological changes, which are primarily important when assessing the arrhythmogenic phenotype.

Most commonly, attention is paid to:

T-wave changes in the inferior leads in a patient with MVP are sometimes referred to as nonspecific ST-T changes associated with prolapse (formerly the term "MVP syndrome" was used). These changes do not correspond to a coronary artery territory and do not prove the absence of ischemia by themselves — when acute coronary syndrome is suspected, ST depression is interpreted separately, taking into account clinical presentation, ECG dynamics, and troponin.

الآلية

During systolic displacement of the leaflet beyond the plane of the mitral annulus, the papillary muscles and chordae are stretched, which creates mechanical tension in the myocardium of the inferoposterior wall of the left ventricle and the papillary muscles. It is hypothesized that such mechanical stress, stretching, and subsequent fibrosis of the papillary muscles and inferobasal myocardium may contribute to repolarization heterogeneity and ventricular ectopy, but the mechanism is multifactorial and arrhythmia does not originate exclusively from these zones in all patients — localization is refined by VE morphology, imaging, and, if necessary, MRI. Pronounced myxomatous degeneration of the leaflets with thickening and excessive chorda tension, as well as mitral annular disjunction (MAD), are associated with greater myocardial electrical instability, which partially explains the link to ventricular arrhythmias in the arrhythmogenic phenotype of MVP.

الأسباب

• Primary prolapse (myxomatous degeneration, Barlow's disease)
• Marfan syndrome and other connective tissue disorders (Ehlers-Danlos)
• Functional mitral regurgitation in ischemic papillary muscle dysfunction or left ventricular dilation is not necessarily true leaflet prolapse, but rather leaflet restriction and displacement
• True secondary prolapse in local damage or rupture of chordae and other structural causes, confirmed by echocardiographic criteria
• Congenital anomalies of the chordal apparatus
• Idiopathic prolapse without structural connective tissue pathology

التشخيص التفريقي

• Inferior wall ischemia: cannot be distinguished from MVP changes by a single ECG; in case of symptoms or doubt, clinical presentation, serial ECGs, and high-sensitivity troponin are evaluated — the presence of MVP does not rule out ACS
• Prior inferior myocardial infarction: look for a pathological Q wave, which is not characteristic of MVP
• Autonomic dysfunction: similar nonspecific T-wave inversion; differentiation requires clinical evaluation, repeat/serial ECGs, consideration of medications and blood electrolytes, and, if indicated, echocardiography to detect MVP and other structural diseases; a causal link between T-wave changes and MVP cannot be established from a single ECG
• Early repolarization syndrome: ST elevation and J-point notching, rather than T-wave inversion
• Hypokalemia: T-wave flattening combined with a U wave and changes in other leads, corrected based on blood potassium

الأهمية السريرية والتكتيكات

In most patients with MVP, the ECG is normal or shows nonspecific changes and does not require separate treatment. It is important for the physician to:

• not interpret T-wave inversion in the inferior leads as ischemia without clinical presentation and dynamics, but also not rule out ACS solely based on known MVP;
• in newly detected ST-T changes and complaints of palpitations or syncope, rule out a structural cause — echocardiography assessing the degree of prolapse, leaflet thickness and redundancy, and mitral regurgitation;
• in frequent or complex ventricular extrasystoles, paroxysms of ventricular tachycardia, syncope, or a family history of sudden death, evaluate for signs of the arrhythmogenic phenotype of MVP (myxomatous, overly mobile leaflets, mitral annular disjunction, inferior T-wave inversion, complex VE/VT) — such patients require urgent evaluation by a cardiologist/arrhythmologist with Holter monitoring, echocardiography, and, when indicated, cardiac MRI; in syncope, sustained or fast SVT/VT, specialized risk stratification for sudden death and consideration of antiarrhythmic therapy, catheter ablation, or implantable cardioverter-defibrillator placement according to current criteria;
• keep in mind that risk factors for sudden cardiac death in MVP include severe myxomatous degeneration and leaflet redundancy, mitral annular disjunction, MRI-detected fibrosis, and complex ventricular extrasystole/VT, but the proportion of such cases among all sudden deaths in MVP cannot be quantified solely by ECG signs — assessment requires a comprehensive examination.

الأخطاء الشائعة أثناء قراءة تخطيط القلب

• Diagnosing MVP by ECG is impossible; confirmation is exclusively echocardiographic
• Mistaking nonspecific T-wave inversion for ischemia and referring for emergency coronary angiography without clinical data, or conversely — ruling out ACS solely based on a history of MVP
• Ignoring frequent or complex ventricular extrasystoles in a patient with known MVP without assessing for signs of the arrhythmogenic phenotype
• Failing to correctly measure QTc when identifying a visually prolonged QT interval by using Bazett's formula without accounting for its inaccuracy in tachycardia and bradycardia
• Confusing ST-T changes in MVP with early repolarization or a normal variant of juvenile T waves

الأسئلة الشائعة

المصطلحات ذات الصلة

المزيد في قسم «التامور، الرئتين، الدماغ وأخرى»

القسم بأكمله

المصادر

• Goldberger A.L. Clinical Electrocardiography, الطبعة الأخيرة
• Surawicz B., Knilans T. Chou's Electrocardiography in Clinical Practice
• أورلوف ف.ن. دليل تخطيط القلب الكهربائي

مادة تعليمية لطلاب كليات الطب والأطباء. لا تحل محل التوصيات السريرية والفحص الطبي؛ يُفسر تخطيط القلب دائماً جنباً إلى جنبกับการحالة السريرية.