|Year : 2019 | Volume
| Issue : 5 | Page : 215-220
Acute myocardial infarction associated with right bundle branch block and changeable trifascicular block: a case report
Yasser Mohammed Hassanain Elsayed
Damietta Health Affairs-Egyptian Ministry of Health, Egypt
|Date of Submission||19-Jun-2019|
|Date of Decision||28-Aug-2019|
|Date of Acceptance||20-Sep-2019|
|Date of Web Publication||01-Oct-2019|
Yasser Mohammed Hassanain Elsayed
Damietta Health Affairs-Egyptian Ministry of Health
Source of Support: None, Conflict of Interest: None
Rationale: Acute myocardial infarction in the presence of right bundle branch block.
Patient concerns: A 70-year-old, male heavy smoker presented with angina and hypertension.
Interventions: Electrocardiography, intravenous nitroglycerin infusion, intravenous streptokinase infusion.
Diagnosis: Acute myocardial infarction in the presence of with changeable trifascicular heart block.
Outcomes: Dramatic clinical improvement with electrocardiographic ST-segment (whether elevation or reciprocal ST-depression) resolution.
Lessons: Acute myocardial infarction may be associated right bundle branch block. Accompanied trifascicular heart block had pre-streptokinase left anterior fascicular block with left axis deviation and post-streptokinase left posterior fascicular block with right axis deviation.
Keywords: Acute myocardial infarction, Anteroseptal myocardial infarction, Right bundle branch block, Changeable trifascicular block
|How to cite this article:|
Elsayed YM. Acute myocardial infarction associated with right bundle branch block and changeable trifascicular block: a case report. J Acute Dis 2019;8:215-20
|How to cite this URL:|
Elsayed YM. Acute myocardial infarction associated with right bundle branch block and changeable trifascicular block: a case report. J Acute Dis [serial online] 2019 [cited 2020 Oct 27];8:215-20. Available from: http://www.jadweb.org/text.asp?2019/8/5/215/268412
| 1. Introduction|| |
Right bundle branch block (RBBB) is defined as a prolongation of QRS duration ≥120 ms, with an rsr’, rsR’, or rSR’ pattern in the lead of V1 or V2 of right chest. The electrocardiographic diagnosis of acute myocardial infarction (AMI) is very difficult if there are associated bundle branch block pattern. RBBB, as a sequel of the acute anterior myocardial infarction (MI), is mostly linked to the proximal of left descending coronary artery (LAD) occlusion with affecting the septal arteries supplying the bundle branches, or the left main coronary artery. RBBB is statistically present in about 6 percent of MIs. Because of the more RBBB in anterior location of the right ventricle than in the left ventricle, stimulation of the right ventricular free wall can equalize the abnormal septal forces of anteroseptal MI. The right bundle branch block traverses the interventricular septum across the cardiac apex. Indeed, damage of the interventricular septum and the RBB mostly occurs by acute anterior myocardial infarction or severe ischemia due to a very proximal left anterior descending artery occlusion. However, most cases of anteroseptal myocardial infarction with classical RBBB associated with pathological Q-waves in right precordial leads (V1-3) is due to delaying in activation of the right ventricle. Left bundle branch block can mask ST-segment deviations because it can mask the repolarization phase changes or Q-waves, while RBBB can not. In rare conditions, the abnormal Q-waves in the anteroseptal may be masked by early depolarization of the right ventricular free wall. Despite the RBBB does not actually mask the repolarization phase or preexisting Q-waves, minor ST-segments elevation in the anterior leads (i.e., V1–V4) may be missed due to the pseudonormalization of the negative T-waves. Anyhow, in the cases of myocardial infarction, the RBBB occurs lonely or in conjunction with left anterior hemiblock (Left anterior fascicular block) or left posterior hemiblock (Left posterior fascicular block. Up till now, the studies did not compare the consequence of new-RBBB and the older one. However, newly-onset and chronic RBBB is an important independent risk factor for future adverse inhospital serious events. The RBBB can be classified according to the onset time, duration, and accompanied fascicular block. RBBB is mostly the finding of large myocardial infarctions.
Interrogatively, the RBBB is not recorded as an indication for reperfusion therapy. Interestingly, broadening QRS-duration with RBBB may indicate great damage for the conduction system including right and left bundles from ischemia or infarction yielding a high opportunity for early aggressive reperfusion or revascularization. Certainly, the current European Society of Cardiology Guidelines suggests a primary percutaneous coronary intervention strategy when persistent ischemic symptoms and RBBB occur in patients, but the level of evidence is not high. Undoubtedly, old studies of thrombolytics have revealed a reduction in infarct size, amelioration in late ventricular morphology and function, and decreasing in mortality,. Early ST-segment elevation restoring post-fibrinolytic therapy despite chronic RBBB is accompanied with reduced death rate.
Indeed, the presence of an RBBB in the association with acute anterior myocardial infarction is accompanied by a higher risk of sudden cardiac death on comparison with that of normal conduction. Whatever, the worse prognosis for the cases of widening QRS-duration with RBBB mostly is due to great damage for the conduction system by ischemia or infarction. Several studies regard the combination of AMI and BBB pose the poorer prognosis than the patients with only AMI,. Many studies had revealed a positive relationship between RBBB and all-cause mortality,,, while others never reported this association,. Regarding the blood supply of the RBB is mainly provided by LAD or the proximal septal perforator branch, the newly-onset RBBB may indicate the proximal occlusion of the LAD and large infarction with subsequent acute heart failure, complete heart block, serious arrhythmia, and a high mortality rate. An anterior AMI with RBBB will increase the QRS-duration, which is accompanied by elevated 30-day mortality.
Trifascicular heart block is the combination of bifascicular block with first-degree heart block. The most important causes of trifascicular heart block are coronary artery disease, anterior myocardial infarction, hypertension, congenital heart disease, primary degenerative disease of the conducting system such as Lenègre-Lev disease, aortic stenosis, drug toxicity such as digitalis and electrolytes imbalance such as hyperkalemia. There are two categories of trifascicular heart block: the first one is incomplete trifascicular heart block; characterized with bifascicular block with first-degree heart block (most common one), bifascicular block with second-degree heart block, and RBBB with alternating left anterior fascicular block/left posterior fascicular block; The second one is complete trifascicular block; characterized with bifascicular block with third-degree AV block. Asymptomatic bifascicular block with first-degree AV block is not an indication for pacing (class III).
| 2. Case report|| |
A 70-year-old male heavy smoker presented with acute severe chest pain, associated with profuse sweating and headache. Informed consent has been signed by the patient. The patient smoked about 60 cigarettes per day for nearly 30 years. He denied the history of the same attack, cardiovascular diseases, drugs or any other special habits. Chest pain had become anginal, compressible, and progressive. Upon general physical examination, the patient was anxious, severe sweaty, with cold extremities, a regular heart rate of 80 bpm, blood pressure of 160/110 mmHg, respiratory rate of 22 bpm, the temperature of 36.7 °C, and pulse oximeter of O2 saturation of 95%. No more relevant clinical data were noted during the clinical examination. He was admitted into the ICU due to anginal chest pain. Urgent ECG was done, which showed complete RBBB, an anteroseptal (V1-3) and high lateral (I , aVL) acute ST-segment elevation myocardial infarction and reciprocal ST-depression changes in leads (II, III, aVF), prolonged PR-interval, sporadic uniformed PVCs (V4-6), left axis deviation, (V1-3) [Figure 1]A, [Figure 1]B, and sinus arrhythmia [Figure 1]A. The case was initially managed as an acute anteroseptal and lateral ST-elevation myocardial infarction in RBBB with a changeable trifascicular block. Sublingual 5-dinitrate tablet (5 mg), O2 inhalation (100%, by nasal cannula, 5 L/min), pethidine HCL 100 mg (on intermittent IV doses), and intravenous nitroglycerin infusion (10 μg/min with intermittent titration) were given. Serial ECG tracings were taken. Aspirin 4 chewable oral tablet (75 mg), clopidogrel 4 oral tablet (75 mg), streptokinase IVI (1.5 million units over 60 min) were added after blood pressure control. Clinical improvement and electrocardiographic ST-segment (whether elevation or reciprocal ST-depression) resolution [Figure 2]A, [Figure 2]B, [Figure 2]C had happened. Serial ECG tracings were taken that showed complete right bundle-branch block, gradual resolution of anteroseptal (V1-3) and high lateral (I , aVL) acute ST-segment elevation myocardial infarction and normalization of reciprocal ST-depression changes in leads (I, III, aVF), prolonged PR-interval, right axis deviation, (V1-3) [Figure 2]A, [Figure 2]B, [Figure 2]C. The measured random blood sugar was 189 mg/dL. Troponin test was positive (385 ng/L). D-dimer was 1 029 ng/mL. Later echocardiography was mild anteroseptal and lateral hypokinesia with ejection fraction of 65%. No more workup was done. The patient was continued on captopril tablet (25 mg twice daily), aspirin tablet (75 mg/d), clopidogrel tablet (75 mg/d), nitroglycerin retard capsule (2.5 mg twice daily), and atorvastatin (40 mg/d) until discharged on the 5th day. Planning for both possible pacing and catheter revascularization was the future option.
|Figure 1. Serial ECG results; A: RBBB, ST-segment elevations in V1-3, I, aVL (red arrows) with Q-wave (black arrows) in V1-3 leads, reciprocal ST-segment depressions in II, III, aVF (green arrows) leads, LAD (lemon and|
purple arrows), prolonged PR-interval (green rectangles) lead II, sinus arrhythmia, and PVCs in V1-3. B: like "A" but with no sinus arrhythmia and PVCs.
Click here to view
|Figure 2. Serial ECG results. A: RBBB, ST-segment resolution in V1-3, I, aVL (green arrows) with increasing the Q-wave (black arrows) in V1-3 leads, RAD (red and purple arrows), prolonged PR-interval (green rectangles) lead II. B: like "A" but with sinus and more increasing the Q-wave (black arrows). C: like "A" with more increasing the Q-wave (black arrows).|
Click here to view
| 3. Discussion|| |
Acute anteroseptal and lateral ST-elevation myocardial infarction in the presence of RBBB with hypertension were the initial presentations. Acute myocardial infarction was associated with changeable trifascicular heart block in the present case. Accompanied trifascicular heart block had pre-streptokinase left anterior fascicular block with left axis deviation and post-streptokinase left posterior fascicular block with right axis deviation. An existence of sporadic premature ventricular contractions [Figure 1]A and sinus arrhythmia [Figure 1]A, [Figure 2]B was benign and insignificant. Typical ischemic chest pain, ST-segment elevation, pathological Q-wave, and positive troponin test are the keys for diagnosis of acute myocardial infarction in this case. Positive d-dimer in the patient may be a marker for associated venous thromboembolism, aortic dissection, and may have a diagnostic role in myocardial infarction in a few studies.
The case was stable through the course of management. This was clearer after controlling of hypertension (nitroglycerin) and acute myocardial infarction with both antiplatelet (aspirin, clopidogrel) and thrombolytic (streptokinase). Proximal of LAD occlusion with the septal arteries are mostly attributed to anteroseptal infarction, but the circumflex artery is involving in high lateral infarction. Asymptomatic trifascicular block without complete heart block is not an indication for pacing (class III). Acute pulmonary embolism, other titles of the acute coronary syndrome, aortic dissection, and acute pericarditis are implicated in the differential diagnosis.
The current case can’t be compared with similar conditions for there is no similar or known cases with the same management. There are no other known limitations in the study, except for contraindications of streptokinase and nitroglycerin are possible limitations. It is recommended to widening the research in clearing the stabilizing effect of streptokinase in the cases of acute myocardial infarction with RBBB.
| 4. Conclusion|| |
Acute myocardial infarction with RBBB has dramatic response to streptokinase. Accompanied trifascicular heart block had pre-streptokinase left anterior fascicular block with left axis deviation and post-streptokinase left posterior fascicular block with right axis deviation. This means a change of axis with thrombolytic therapy. Trifascicular heart block is an extreme association. It may be changeable and benign that does not indicate further intervention.
Conflict of interest statement
The authors report no conflict of interest.
The author wishes to thank the critical care unit nurses who made extra ECG copy for helping.
| References|| |
Wong CK, Gao W, Stewart RA, van Pelt N, French JK, Aylward PE, et al. Risk stratification of patients with acute anterior myocardial infarction and right bundle-branch block: importance of QRS duration and early ST-segment resolution after fibrinolytic therapy. Circulation
(8): 783-789. DOI:10.1161/CIRCULATIONAHA.106.639039.
Mishra V, Sinha SK, Razi M. Right bundle branch block: A masquerader in acute coronary syndrome. N Am J Med Sci
(2): 121-122. DOI: 10.4103/1947-2714.177347.
Wong CK, Stewart RA, Gao W, French JK, Raffel C, White HD. Prognostic differences between different types of bundle branch block during the early phase of acute myocardial infarction: insights from the Hirulog and Early Reperfusion or Occlusion (HERO)-2 trial. Eur Heart J
(1): 21-28. DOI:10.1093/eurheartj/ehi622.
Rosenbaum MB, Girotti LA, Lázzari JO, Halpern MS, Elizari MV. Abnormal Q waves in right sided chest leads provoked by onset of right bundle-branch block in patients with anteroseptal infarction. Br Heart J
(3): 227-232. DOI:10.1136/hrt.47.3.227.
Wang J, Luo H, Kong C, Dong S, Li J, Yu H, et al. Prognostic value of new-onset right bundle-branch block in acute myocardial infarction patients: a systematic review and meta-analysis. Peer J
Bhalli MA, Khan MQ, Samore NA, Mehreen S. Frequency and clinical outcome in conduction defects in acute myocardial infarction. J Ayub Med Coll Abbottabad
Wang JT, Zhu JL, Luo HX, Kong CL, Zhang C, Chu YJ. Diagnosis, prognostic significance, and characteristics of new-onset right bundle-branch block in patients with acute myocardial infarction: Protocol for a systematic review and meta-analysis. Curr Res Cardiol
Kleemann T, Juenger C, Gitt AK, Schiele R, Schneider S, Senges J, et al. Incidence and clinical impact of right bundle branch block in patients with acute myocardial infarction: ST elevation myocardial infarction versus non-ST elevation myocardial infarction. Am Heart J
Widimsky P, Rohác F, Stásek J, Kala P, Rokyta R, Kuzmanov B, et al. Primary angioplasty in acute myocardial infarction with right bundle branch block: should new onset right bundle branch block be added to future guidelines as an indication for reperfusion therapy? Eur Heart J
(1): 86-95. DOI:10.1093/eurheartj/ehr291.
Archbold RA, Sayer JW, Ray S, Wilkinson P, Ranjadayalan K, Timmis AD. Frequency and prognostic implications of conduction defects in acute myocardial infarction since the introduction of thrombolytic therapy. Eur Heart J
(6): 893-898. DOI:10.1053/euhj.1997.0857.
Juarez-Herrera U, Jerjes-Sanchez C. Risk factors, therapeutic approaches, and in-hospital outcomes in Mexicans with ST-elevation acute myocardial infarction: The RENASICA II multicenter registry. Clin Cardiol
(5): 241-248. DOI:10.1002/clc.22107.
Reihani H, Shamloo AS, Keshmiri A. Diagnostic value of d-dimer in acute myocardial infarction among patients with suspected acute coronary syndrome. Cardiol Res
(1): 17-21. DOI: 10.14740/ cr620w.
[Figure 1], [Figure 2]