• 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • br Commentary Careful analysis of the electrocardiograph Fig


    Commentary Careful analysis of the electrocardiograph (Fig. 1) reveals narrow and similar QRS complexes in all the beats, showing that they are all intrinsic QRS complexes. Some intrinsic P waves are also visible at the ST-T segment (after R3, R7, R11, and R15); these are the beats without any spike before them. The baseline rhythm is therefore an accelerated junctional rhythm. Some atrial spikes generate P waves (a P wave is clearly visible in R6, especially in lead V1, and with careful attention, it may be seen in beats R1, R4, R5, R8, R9, R12, R13, and R16). These points rule out atrial lead dislodgment into the right ventricle or reverse connection of the atrial and ventricular leads. In R2, R6, R10, and R14, a very short interval between atrial and ventricular spikes is seen, which is because of the ventricular safety pacing (VSP) parameter being activated in the device. In Medtronic devices, when this option is on, a sensed signal during the VSP window and after PAVBP triggers ventricular stimulation at the end of the VSP window (Fig. 2). This feature is designed to prevent ventricular inhibition caused by crosstalk of the atrial spike [1]. If an intrinsic ventricular beat happens exactly after PAVBP, and the pAVI delay setting is prolonged, a spike on the T wave may be induced. However, if the safety pacing is on, pAVI is shortened to 110ms, avoiding cross talk and the spike on the T wave. In these beats, as the rate of the underlying rhythm was close to the pacing rate, simultaneous atrial pacing and sensed intrinsic QRS caused earlier ventricular pacing. As these stimuli followed too close to the preceding intrinsic QRS complex, they occurred during the ventricular myocardial refractory period and did not produce any QRS complexes.
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    Case presentation A 72-year-old woman was admitted to the emergency department because of chest pain. She was on valsartan 160mg daily for hypertension. Physical examination on admission was unremarkable. Twelve-lead electrocardiogram (ECG) revealed sinus rhythm (92bpm) with diffuse ST-segment depression (involving eight leads) associated with ST-segment elevation in lead aVR (Fig. 1). In addition, ECG showed rightward mean frontal plane QRS-axis and R-wave beta adrenergic blockers with pure R waves in leads V1–V3 suggesting right ventricular pressure or volume overload. The patient had no history of chronic obstructive pulmonary disease, rheumatic valvular disease, or other conditions indicating right ventricular pathology. Cardiac enzyme levels were elevated: Creatine kinase (CK)-MB at 7.9ng/ml (0.6–6.3ng/ml) and troponin I at 0.79ng/ml (0–0.04ng/ml). Since the elevated levels of the cardiac enzymes and ECG changes indicated left main coronary artery or three‐vessel disease, coronary angiography was performed. Surprisingly, it was normal. Bedside echocardiography showed right ventricular enlargement with a normal left ventricular ejection fraction (60%). Computed tomography of the chest was performed because of suspicion of acute pulmonary embolism (APE), and it revealed a thrombus in the right pulmonary artery (Fig. 2). Therefore, thrombolytic therapy (alteplase) was started, and the patient was discharged six days after admission. Clinical symptoms may be similar in patients with acute coronary syndrome (ACS) and APE, and biochemical markers of myocardial necrosis may be elevated in both diseases. In addition to the medical history and clinical and laboratory findings, 12-lead ECG is important, but has some limitations in the differential diagnosis of ACS and PE. ECG changes suggestive of myocardial ischemia were observed in 70% of patients with APE, and predicted worse progression and 30-day mortality [1,2]. Diffuse ST-segment depressions in more than six leads associated with ST-segment elevation in aVR lead has been associated with left main, left main equivalent, or severe three‐vessel disease [3]. ST-segment elevation in lead aVR may also occur in APE patients, probably as an expression of right ventricular overload or right ventricular ischemia. It is associated with poor prognosis [4,5]. A similar case of APE with diffuse ST-segment depressions in more than six leads associated with ST-segment elevation in aVR lead was reported before [6]. To the best of our knowledge, our case is the second one in the literature related to this issue. Emergency physicians, cardiologists, and internists should be aware of the ECG findings of APE mimicking ACS.