There is a phenomenon of electrical alternation not only QRS complex, but also T-wave macro-alternans mainly in V1-V4 lead ECG. Electrical alternans is a broad term that describes alternate-beat variation in the direction, amplitude, and duration of any component of the ECG waveform (ie, P, PR, QRS, R-R, ST, T, U). Electrical alternans associated with cardiac motion is due to alternation in the position of the heart with relation to recording electrodes.

T-wave alternans has been reported with congenital long QT syndrome, electrolyte imbalances (eg, hypocalcemia, hypokalemia, hypomagnesemia), treatment with quinidine or amiodarone , hypertrophic cardiomyopathy, alcoholic cardiomyopathy, congestive heart failure, and acute pulmonary embolism. T-wave alternans has also been reported following cardiac resuscitation. Most importantly, the presence of T-wave alternans can be used as a predictor of ventricular tachyarrhythmic events, such as sudden cardiac death, sustained ventricular tachycardia, ventricular fibrillation, implantable cardioverter defibrillator (ICD) therapy, and cardiac arrest.

Manifestation of alternation QRS complex on the surface ECG may be seen in the setting of myocardial ischemia, rheumatic heart disease, acute pulmonary embolism, myocardial contusion, and left ventricular dysfunction. The most common underlying disorder is an enlarged pericardial effusion or presence of pericardial disease (upon detection both electrical alternans such as QRS and T- wave), frequently suggests cardiac tamponade, but total electrical alternans is seen in only 5-10% of patients with cardiac tamponade. Heart movement in patients with hypertrophic cardiomyopathy or noncompact myocardial syndrome also may result in electrical alternans of this type.

There might be far more simpler explanation given the nature of the changes you show; simply movement towards and away from the chest wall by the heart in respiration. The progressive periodicity you show (especially in V3) is diagnostic). And while electrical alternans is a compelling answer, that EKG isn’t electrical alternans-but it was a very nice description however.

Thank you Tatiyana for for your detailed discussion. But I think the change in the amplitude of the QRS is related to the respiratory movements as suggested by Robert. It is not too infrequent to find this ECG phenomenon in our day to day practice in patients who have no structural heart disease. However it is good to consider the various situations which have been pointed out in the background of the clinical context. Moreover, the ECG pattern is not typical of "electrical alternans" .

Thank you for all your answers !

Let me introduce this case briefly:

M,67 y

Chief complaint: Dyspnea on exertion for 10 years, chest pain for half year and be exacerbated for 2 days.

Past history:Hypertension for 20 years ,Max BP 170/90mmHg

History of present illness:The man felt chest pain after exercise one morning，so he went to ER，EKG is nearly normal ，cTNI 0.022ng/ml，while waiting for doctor,he lost consciousness and AS occurred，immediate EKG showed VF，so we defibrillated several times and EKG restore sinus rhythm，repeated cTNI 18.3ng/ml.The EKG I provided previously was recorded after defibrillation.The patient was immediately done enhanced chest CT to exclude PE and dissection.After that, coronary arteriongraphy was done .To our surprise,CAG showed normal coronary arteries except myocardial bridge lies on LAD and the myocardial bridge just pinch the LAD slightly.LVG showed normal shaped LV，so we exclude Takotsubo cardiomyopathy although abdominal CT showed multiple nodules on bilateral adrenal .Echocardiography showed hypokinetic on Inf. wall and apex，LVEF 35%.Finally CMR showed myocardial edema、necrosis and microhaemorrhages on defined region ,not diffuse(I have forgotten the exact region...). In summary,we excluded cardiomyopathy、myocarditis and gave the diagnosis of MINOCA.

Dear Colleagues

Thank you for an interesting case and no less instructive discussion.

Dr. Andrei G Dan, you are always very persuasive, and I'm ready to subscribe under each your item.

However I just want to add my opinion about the possible effects of muscular bridge (MB) in the development of this dramatic situation

1.Since described by Cranicianu in 1922, MB has been widely investigated. Though it has been regarded to be benign, I such as many colleagues convinced that MB may be an anatomic risk factor for coronary atherosclerosis and myocardial infarction. Furthermore, MB can lead to myocardial ischemia, infarction, ventricular tachycardia, ventricular fibrillation and sudden cardiac death.

2. Acute ischemia occurs when the supply of myocardial blood flow is inadequate compared with the demand. It usually occurs in the setting of coronary arteriosclerosis and coronary spasm. Though MB has long been regarded as a variant without hemodynamic or physiological relevance, recent researches have shown that MB can impair coronary blood flow.

3. Corrado D. et al. reported that in their study, among 16 sudden cardiac deaths with aged under 35 years caused by non-atherosclerotic coronary diseases, six cases were founded to have MB in the LAD. In addition, MB can lead to sudden death among of the young athlete such as basketball and football players. These studies indicated that MB may be a cause of sudden cardiac death among individuals without coronary atherosclerosis, which seemed superficially healthy.

4. In present case, after episodes of chest pain, 67-year patient suffered episode of cardiac arrest, which may be associated with MB in the LAD. Possibly, there existed an abnormal coronary flow reserve in the site distal to the bridged segment and exercise increased the demand and decreased the of myocardial blood flow, which intensified myocardial supply/demand mismatch and leaded to acute ischemia/MI

5. ...alternation QRS complex on the surface ECG may be seen to both myocardial ischemia and vector changes after defibrillation ....artifact is questionable, since it is limited to two leads and the localization is corresponding MB

Thanks for the clinical details. It appears to be an ACS and the cardiac arrest consequent to primary VF. The myocardial bridge is in the LAD and echo and CMR show abnormalities in the inferior wall. It is possible with wrap around type 3 LAD but there are no wall motion abnormalities in the LAD territory. The ECG shows small a in Lead 3 and small initial r in V1 and V2 with minor T inversions. The ECG does not suggest a STEMI. Serial EGGs could have helped. It seems that the entire picture is that of ACS with recanalised coordinators and may be (?) Incidental myocardial bridge. But it is difficult to relate the change in QRS amplitude to the clinical scenario.

Hi Tatiyana, Dr Koshy, Dr Dan Dr Hua.. Thanks everyone for very nice and elaborative discussion.. It was probably a case of acute coronary syndrome with relatively normal coronaries. Myocardial bridge can cause arrhythmia but I doubt strongly in this case as a cause of VT. Presence of bilateral nodule in adrenal seems interesting in this case. What was the serum potassium level in this patient. Because hypokalemia and hyperkalemia both can cause VT and adrenal pathology can cause both.. Thanks

Hi,Dr Majumder.The patient`s electrolytes in blood was normal.We have tested the ACTH and cortisol in blood which were normal in quantity and in circadian rhythm.But it is a pity that labs of our hospital have no method to do the blood test of aldosterone and catecholamines!So aldosteronism and pheochromocytoma can`t be completely ruled out although in my opinion bilateral nodules in adrenal seem low correlation with ACS and maybe more correlation with hypertension.

I will upload CAG、LVG animation and CMRI report next few days.

I have uploaded CAG and LVG animation of this patient.

this is depending on the position of the lead

More likely it is amplitude changes due to increased thoracic impedance as a measure of respiratory variation as we mention above....Occam's Razor.