Revista medica del Instituto Mexicano del Seguro Social · 2025
[Wolff-Parkinson-White syndrome due to cocaine use: a case report].
Клинический случайАннотация на английскомСтатьяНазвание и аннотация: Перевод в очереди
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Lara-Duck Manlio Fabio, Rosales-Martínez Juan, Mayek-Pérez Netzahualcoyotl
Аннотация
BACKGROUND: Wolff-Parkinson-White syndrome (WPWS) causes an accessory pathway between the atria and ventricles, in parallel with the atrioventricular node and the bundle of His; it causes a "short circuit" that deregulates the physiological pacing and causes tachycardia. A case of WPWS is described in a patient with cocaine, alcohol, and tobacco consumption.
CLINICAL CASE: A 34-year-old man with a regular history of cocaine, alcohol, and tobacco use for 14 years presented with paroxysmal palpitations, chest pain, and shortness of breath. ECG 1 revealed supraventricular tachycardia with delta waves and a short P-R interval; ECG 2 revealed reversal of the tachycardia without delta waves and inverted T waves in lead 1, aVR, and aVL, and a short P-R interval; ECG 3 revealed sinus rhythm, 90 bpm, and inverted T waves in lead 3, aVR, and v1. TTE showed a normal left ventricle; a normal LVEF, greater than 50% (Simpson's method); and no stenosis or regurgitation in the mitral, tricuspid, and mitral valves. 24-hour Holter monitoring revealed non-sustained paroxysmal supraventricular tachycardia, with a narrow QRS complex, a short P-R, interval of 122 bpm, and T wave inversion during paroxysm. Reversal of paroxysm maintained a short P-R and normal T waves.
CONCLUSIONS: Upon reversal of the patient's supraventricular tachycardia paroxysms, his T waves corrected (positive T waves). The inverted T waves were due to WPWS, triggered by cocaine, alcohol, and tobacco use, and possibly related to myocardial ischemic involvement.
CLINICAL CASE: A 34-year-old man with a regular history of cocaine, alcohol, and tobacco use for 14 years presented with paroxysmal palpitations, chest pain, and shortness of breath. ECG 1 revealed supraventricular tachycardia with delta waves and a short P-R interval; ECG 2 revealed reversal of the tachycardia without delta waves and inverted T waves in lead 1, aVR, and aVL, and a short P-R interval; ECG 3 revealed sinus rhythm, 90 bpm, and inverted T waves in lead 3, aVR, and v1. TTE showed a normal left ventricle; a normal LVEF, greater than 50% (Simpson's method); and no stenosis or regurgitation in the mitral, tricuspid, and mitral valves. 24-hour Holter monitoring revealed non-sustained paroxysmal supraventricular tachycardia, with a narrow QRS complex, a short P-R, interval of 122 bpm, and T wave inversion during paroxysm. Reversal of paroxysm maintained a short P-R and normal T waves.
CONCLUSIONS: Upon reversal of the patient's supraventricular tachycardia paroxysms, his T waves corrected (positive T waves). The inverted T waves were due to WPWS, triggered by cocaine, alcohol, and tobacco use, and possibly related to myocardial ischemic involvement.