ST segment elevation in anterior precordial leads and right ventricular infarction. Apropos of 6 cases]

ST segment elevation in the anterior precordial chest leads may be observed in some cases of right ventricular infarction alone or associated with left ventricular inferior wall infarction. Six out of 700 patients admitted to our Coronary Care Unit over a 2 year period had right ventricular infarction with these electrocardiographic changes. In three cases, isolated right ventricular infarction was due to occlusion of a right marginal artery (N = 2) or of a small right coronary artery (N = 1) which only vascularised the right ventricle. In 2 cases, right ventricular infarction was associated with a recent or chronic left ventricular inferior wall infarct. This type of ST segment elevation may suggest a left ventricular anterior wall infarct especially when there are no changes in the inferior leads, as was the case in our first patient. However, the dome-like appearance of the ST segment, the reduction in amplitude of ST elevation from V2 to V5, the progressive regression of the ST changes without the appearance of Q waves, are more suggestive of the diagnosis of right ventricular infarction. In addition, normal left ventricular dilatation on echocardiographic examination rapidly confirms the diagnosis.     

Right ventricular cardiomyopathy showing right bundle branch block and right precordial ST segment elevation

A 73-year-old man who had a family history of sudden death, experienced syncope. His electrocardiogram (ECG) presented right bundle branch block and right precordial ST segment elevation which are findings identical with those in Brugada syndrome. The cardiac MRI showed right ventricular mild dilatation, and endomyocardial biopsy revealed fatty replacement of myocardial fibers. Though no ventricular tachyarrhythmias were induced during an electrophysiologic test, the effects on ECG of antiarrhythmic agents and autonomic modulations were similar to those in Brugada syndrome. This case may suggest the relationship between Brugada syndrome and right ventricular cardiomyopathy.     

Right precordial ST and QRS changes in the diagnosis of right ventricular infarction

Two groups of patients with anatomically proved acute myocardial infarction were compared in order to study specificity and sensitivity of the ECG criteria previously described in clinical and experimental right ventricular infarction ( RVI ). Group 1 included 21 patients with left inferior infarction and with a variable degree of right ventricular involvement; group 2 included nine patients with myocardial infarction confined to the left inferior wall. In both groups the presence of ST elevation (at least 0.05 mV) and the morphology of the QRS complex in V4R , V3R, and V1 were assessed in ECGs performed at the time of admission. Also, in order to evaluate the morphology of the ST segment and QRS complex in right precordial leads in normal subjects, an ECG with 12 standard and four right precordial leads ( V6R to V3R) was performed in 82 subjects (group 3) without clinical and ECG evidence of heart disease. Our data reveal that in normal subjects an rS pattern is always present in V3R and frequently (91%) in V4R . On the contrary, the presence of QS or QR complexes in both V4R and V3R are specific markers of right ventricular necrosis (specificity 100%; sensitivity 78%). The presence of injury and necrosis waves in V4R or V4R to V3R during inferior infarction is a useful diagnostic criterion in that it insures a highly specific diagnosis of acute RVI in the great majority (76 and 71%, respectively) of the cases with autopsy evidence of right ventricular involvement.     

Massive ST-segment elevation in precordial and inferior leads in right ventricular myocardial infarction

This report describes a case of right ventricular infarction in which massive ST-segment elevation in the precordial and inferior leads was observed. The maximum magnitude of the ST-segment elevation in the precordial leads was 21 mm in lead V2 and that in the inferior leads was 10 mm in lead II. Angiography revealed a reduction of 90% in the diameter of the right coronary artery in its proximal portion and a normal left coronary system. Recent reports have shown that precordial ST-segment elevation may reflect right ventricular infarction. However, no previously reported instance except our case has shown massive ST-segment elevation in both the precordial and inferior leads. In right ventricular infarction, the current of injury is usually simultaneously present in the right ventricular free wall and left ventricular inferior wall, electrically opposed to each other. Thus, the diffuse and massive ST-segment elevation observed in this study seems to be a rare phenomenon.     

Right ventricular infarction/ischemia with precordial ST elevation: comparison with left ventricular anterior wall infarction]

Acute right ventricular (RV) infarction is sometimes accompanied by precordial ST elevation which is also suggestive of left ventricular (LV) anterior wall infarction. We compared 12-lead electrocardiograms between 2 groups of patients with initial acute myocardial infarction presenting precordial ST elevation, one with RV infarction (n = 11) and the other with LV anterior wall infarction (n = 42). The magnitude and extent of the ST elevation and the positions presenting the maximal ST elevation in the precordial leads differed between the 2 groups. In the inferior and lateral leads, the analysis of the ST segment shift aided in distinguishing between the 2 groups. The specific patterns of intraventricular conduction delay and frontal QRS-axis deviation were also useful for the differentiation. The best electrocardiographic variable for identifying RV infarction was inferior lead ST elevation, followed by maximal precordial ST elevation in lead V1, ST elevation limited to only one precordial lead and a cove-shaped pattern of RV conduction delay. The best electrocardiographic predictor for diagnosing LV anterior wall infarction was an isoelectric or depressed ST-segment in the inferior leads, followed by precordial ST elevation equal to or greater than 5 mm, maximal ST elevation in lead V3 or V4 and ST elevation in the lateral leads. We concluded that systematic analysis of the 12-lead electrocardiograms recorded in the hyperacute stage is valuable for distinguishing between acute RV infarction and LV anterior wall infarction.     

ST elevation in the anterior precordial leads during right ventricular infarction: lessons learned during primary coronary angioplasty--a case report.

ST elevation in the anterior leads may be due to isolated right ventricular infarction associated with occlusion of a nondominant or codominant right coronary artery. The authors report a case of isolated right ventricular infarction from a dominant right coronary artery's proximal occlusion in the presence of collateral circulation provided by the left coronary artery. Extensive damage occurred owing to compromise of the collateral circulation during primary coronary angioplasty. This is an unusual angiographic pattern for isolated right ventricular infarction. The potential consequences of percutaneous interventions to collateral vessels is discussed.     

Transient but marked ST elevation in precordial leads caused by ischemia of the isolated right ventricular branch

The present case is a 64 year-old man in whom transient but marked ST elevation was confirmed in the contralateral precordial leads (V1-3) during percutaneous transluminal coronary angioplasty (PTCA) of the proximal right coronary artery, suggesting that the patient had anteroseptal ischemia. The ST elevation persisted even after the balloon was deflated, and no changes in the left coronary artery were detected. In addition, blood flow in the affected area of the right coronary artery was favorable and there was a transient delay only in the right ventricular branch. Once blood flow in the right ventricular branch improved, ST returned to baseline, and when the right ventricular branch was again occluded by the balloon, ST elevation occurred in a reproducible manner. Hence, the electrocardiographic changes in the precordial leads were caused by occlusion of the right ventricular branch. It is rare to observe ST elevation caused by isolated right ventricular branch ischemia.     

Detection of acute right ventricular infarction by right precordial electrocardiography

The value of 0.1 mV or greater of S-T segment elevation in at least one right precordial lead (V₄R to V₆R) in defining right ventricular myocardial infarction was assessed prospectively in 43 subjects (33 consecutive patients with enzymatically confirmed infarction of varying type and location, 4 patients with unstable angina and 6 healthy volunteers). Patients with acute myocardial infarction were studied with radionuclide ventriculography and technetium-99m stannous pyrophosphate myocardial scintigraphy 18.2 ± 14.3 (mean ± standard deviation) and 85.1 ± 18.0 hours after the onset of symptoms, respectively. Eleven patients (Group A: 9 patients with transmural inferior infarction, 1 with transmural inferolateral infarction and 1 with transmural anteroseptal infarction) demonstrated right precordial S-T segment elevation and 22 patients (Group B: 6 patients with transmural inferior infarction, 2 with transmural posterior infarction, 3 with transmural inferolateral infarction, 3 with transmural anteroseptal infarction, 3 with transmural extensive anterior infarction, 4 with subendocardial anterior infarction and 1 with unclassified infarction) did not. Right ventricular ejection fraction was significantly lower in Group A (0.47 ± 0.11) than in Group B (0.60 ± 0.12) (p < 0.01). Right ventricular total wall motion score was 63.8 ± 15.6 percent of normal in Group A versus 94.3 ± 8.5 percent in Group B (p < 0.001). Technetium-99m pyrophosphate uptake (2+ or greater) over the right ventricle occurred in nine patients (81.8 percent) in Group A and in one patient (4.5 percent) in Group B (p < 0.001). No patient with unstable angina and no healthy volunteer had S-T segment elevation in a right precordial lead. S-T segment elevation of 0.1 mV or greater in one or more of leads V₄R to V₆R is both highly sensitive (90 percent) and specific (91 percent) in identifying acute right ventricular infarction.     

Proximal right coronary artery occlusion with ST elevation in all precordial leads

We present a case of a 55-year-old-man with acute coronary syndrome due to occlusion of the right coronary artery. Electrocardiogram showed ST-segment elevation in nine leads. We explain the causes of this exceptional electrocardiographic pattern.     

Marked ST-segment elevation in the precordial and inferior leads in right ventricular myocardial infarction: a case report

This is a report of right ventricular infarction complicated by inferior myocardial infarction in which marked ST-segment elevation was observed in the precordial and inferior leads. A 51-year-old man was admitted with chest pain of one-half hour duration. His admission ECG showed conspicuous ST-segment elevation in the precordial and inferior leads. The maximum magnitude of the ST-segment elevation in the precordial leads was 21 mm in lead V2 and 10 mm in lead II. Echocardiography showed akinesis of the right ventricular free wall and the posterior half of the left ventricle. Angiography revealed a 90% reduction in the diameter of the right coronary artery in its proximal portion, and a normal left coronary system. Recent reports have indicated that precordial ST-segment elevation may reflect right ventricular infarction. However, there has been no previous report of marked ST-segment elevation in the precordial and inferior leads. In right ventricular infarction, the currents of injury usually occur simultaneously in the right ventricular free wall and left ventricular inferior wall, and then are electrically opposed to each other. The diffuse and marked ST-segment elevation observed in this case is thus a rare phenomenon.     

急性下壁心肌梗死心电图胸前导联V1-3 ST段抬高的临床意义

目的 探讨急性下壁心肌梗死患者心电图胸前导联ST段抬高与冠状动脉造影所示冠状动脉病变的关系及其临床意义.方法 187例急性下壁心肌梗死患者,按入院时18导心电图胸前导联ST段改变分为2组,ST段抬高组（16例）和非ST段压低组（171例）.所有患者均行冠状动脉造影术,病变适合行经皮腔冠状动脉成型术并检测B型钠尿肽（BNP）.结果 急性下壁心肌梗死伴胸前导联ST段抬高时多为右冠状动脉近段闭塞,尤其是圆锥支闭塞（P＜0.01）,且伴有右心功能不全和血流动力学障碍,与下壁右室心梗相比BNP差异有统计学意义（P＜0.01）.结论 急性下壁心肌梗死合并胸前导联ST抬高表明为右冠状动脉近段或开口闭塞且多伴右室心肌梗死和心功能不全.     

Exercise-induced ST elevation in patients with arrhythmogenic right ventricular dysplasia

To test the hypothesis that local or diffuse wall motion abnormalities in the right ventricle in patients with arrhythmogenic right ventricular dysplasia (ARVD) may induce the ST-segment elevation in response to exercise, we examined exercise electrocardiograms in patients with ARVD. In 17 patients with ARVD, who demonstrated right ventricular wall motion abnormalities without organic coronary lesions, we conducted a treadmill exercise test. Significant exercise-induced ST-segment elevation (ESTE) was defined as a 0.1 mV or more ST-segment elevation at J point. ESTE was observed in 11 patients (65%). It manifested most frequently in right-sided precordial leads. Severe right ventricular asynergy was seen in all but one (91%) among 11 with ESTE, whereas it was seen only in two (33%) among six without ESTE (P<.05). The maximal magnitude of ESTE inversely correlated with right ventricular ejection fraction (r = -0.58, P<.05). ESTE was seen in two thirds of ARVD patients, helping us noninvasively diagnose ARVD. The fact that ventricular wall motion abnormalities could cause ESTE in the absence of organic coronary lesions suggested the critical role of mechanical factors in the genesis of ESTE.     

急性下壁心肌梗死ST段抬高STⅢ/Ⅱ＞1对右室梗死的诊断价值

目的　探讨ST段抬高STⅢ /Ⅱ >1在急性下壁心肌梗死并发右室梗死的诊断价值。方法　描记常规 12导联和V3R～V7R,以连续 2个QRS波群的TP连线为基线 ,测量Ⅱ ,Ⅲ ,V3R V7R导联J点后 80ms处ST段抬高的幅度。结果　Ⅲ导联ST段抬高 >0 1mv ,且STⅢ /Ⅱ >1者占 2 4例 ,其中 18例 (75 % )并发右室梗死 ;而STⅢ /Ⅱ≤ 1者 2 4例中仅 2例 (8 3% )并发右室梗死 ,二者之间差异显著 (P <0 0 0 1)。其敏感性 ,特异性和准确率分别为 90 %、78%、77%。结论　急性下壁心肌梗死的早期 ,ST段抬高 ,STⅢ /Ⅱ >1,是心电图早期识别合并右室梗死的可靠指标。该指标对诊断右室梗死的敏感性同STV4R段抬高相当     

ST segment elevation in the right precordial leads following administration of class Ic antiarrhythmic drugs

Electrocardiographic changes were evaluated retrospectively in five patients without previous episodes of syncope or ventricular fibrillation who developed abnormal ST segment elevation mimicking the Brugada syndrome in leads V1-V3 after the administration of class Ic antiarrhythmic drugs. Pilsicainide (four patients) or flecainide (one patient) were administered orally for the treatment of symptomatic paroxysmal atrial fibrillation or premature atrial contractions. The QRS duration, QTc, and JT intervals on 12 lead surface ECG before administration of these drugs were all within normal range. After administration of the drugs, coved-type ST segment elevation in the right precordial leads was observed with mild QRS prolongation, but there were no apparent changes in JT intervals. No serious arrhythmias were observed during the follow up periods. Since ST segment elevation with mild QRS prolongation was observed with both pilsicainide and flecainide, strong sodium channel blocking effects in the depolarisation may have been the main factors responsible for the ECG changes. As the relation between ST segment elevation and the incidence of serious arrhythmias has not yet been sufficiently clarified, electrocardiographic changes should be closely monitored whenever class Ic drugs are given.