A patient at handed with an acute right ventricular infarction characterized through an electrocardiographic current of injury in the pair the inferior (2.

A patient at handed with an acute right ventricular infarction characterized through an electrocardiographic current of injury in the pair the inferior (2,3,aVF) and anterior precordial leads ([Vsub1]-[Vsub6]) Cardiac catherization demonstrated normal left ventricular wall motion, a codominant circulation, and strait-laced disease of the right coronary artery. We move that this coronary anatomy explains the injury populars on the electrocardiogram. This case illustrates a rare presentation of right ventricular myocardial infarction mimicking an extensive anterolateral wall injury.

Right ventricular myocardial infarction (RVMI) has been reported to take place in 30 to 40 percent of patients with electrocardiographic evidence of interior-posterior infarction.[1] The importance of recognizing injury of the right ventricle has been emphasized in modern years as the treatment of these patients at times differs from those with predominant left ventricular infarction.[2]

Electrocardiography is a useful tool that may provide rapid diagnosis of RVMI.[3-7] This report chronicles a patient with an unusual electrocardiographic manifestation of right ventricular infarction in the neighborhood of an inferior myocardial infarction.

CASE REPORT

A 51-year-old man, with no history of coronary atherosclerosis at handed to our emergency department with 2-h symptoms of persistent precordial hurry associated with breathlessness, nausea, and diaphoresis. An electrocardiogram revealed an injury present in the inferior and anterior precordial leads [Vsub1]-[Vsub6] A modified [Vsub4]R lead revealed evidence of RVMI (Fig 1)

A diagnosis of acute myocardial infarction was made and the patient was treated with a thrombolytic agent (intravenous Antistreplase [APSAC] 30 U) oral aspirin, 325 mg and intravenous metoprolol tartrate (Lopressor), nitrates, and heparin. The patient's symptoms resolv within an hour of the administration of therapy. Cardiac enzyme analysis confirmed a myocardial infarction, and showed an early peaking creatine kinase value of 1445 (5 percent MB) at 10 h from the first brunt of symptoms. Sequential electrocardiograms revealed resolution of the ST portion elevations and absent Q waves in the anterior leads. A radionuclide ventriculogram performed prior to hospital discharge showed an akinetic right ventricular apex and normal left ventricular function.

Cardiac catheterization performed forward day 5 of hospital admission showed normal left heart compressings Coronary angiography revealed a left coronary artery clear of significant atherosclerosis. The coronary plan displayed codominance with the left circumflex artery supplying a portion of the inferior-posterior left ventricular myocardium. There was 60 percent stenosis of the midright coronary artery that supplies the inferoseptal left ventricular myocardium (Fig 2) A large right ventricular branch with extensive anterior distribution beyond the breastbone revealed a critical stenosis in its proximal part (Fig 3). The left ventriculogram showed normal wall motions.

DISCUSSION

Erdhart and Sjogren[3] first reported the value of monitoring right precordial leads in right ventricular infarction. following studies have confirmed that detection of greater than 1-mm ST portion elevation in lead [V.sub.4]R is a highly specific market for right ventricular necrosis.[3,4] These studies have also documented the transient nature of these ST changes, and thus its limitation in diagnosing RVMI.[5,6]

Chou and Bel-Kahn[5] first described patients with RVMI who manifested anterior precordial ST part elevation in the electrocardiogram. In a series of 64 patients with RVMI, Geft and associates[6] reported that no other than a minority (five patients) exhibited an injury circulating in the left precordial leads. These studies have also noted that the anterior ST elevations in RVMI rarely lengthen out beyond lead [V.sub.4]. no other than 1 of 11 patients described by the agency of Chou and Bel-Kahn[5] exhibited ST elevation in lead [Vsub4] and 2 patients in the series reported by the agency of Geft et al[6] manifested an injury in every one's mouth in lead [V.sub.5].

Geft and coworkers[6] have also emphasized that the magnitude of precordial ST elevation in RVMI decreases from right to left ([Vsub1] to [Vsub4]) and recommend that this decrement in ST elevation, in addition to the absence of Q waves in these leads, may be helpful in differentiating a right ventricular infarction from an anterior left ventricular infarction.

The summation of sum of two units opposing electrical vectors, the anterior injury circulating of RVMI and the posterior electrical forces of simultaneous inferoposterior infarction, may explain the rare proceeding of anterior ST elevation in RVMI. In the majority of cases of RVMI, the inferoposterior injury circulating s of the thicker-walled left ventricle overwhelms the anterior ST portion vector of RVMI, leading to either isoelectric or ST depressions in the left precordial leads. Thus, in the series of Geft et al,[6] those patients with absent precordial ST elevation manifested a marked now passing of injury in the inferior leads, while the five patients with anterior ST elevation exhibited merely small or absent inferior ST portion elevation in the electrocardiogram. Likewise, a patient with a previous inferior infarction who meet withs a subsequent right ventricular infarction, based onward this mechanism of opposing electrical vectors, would be calculate uponed to manifest marked anterior ST elevations in succession the electrocardiogram.[7]

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