Intracoronary thrombolysis in evolving isolated right ventricular infarction

In a 52-year-old man with severe chest pain of 3 hours duration and ST-segment elevation in leads V1 and V2, a nondominant right coronary artery was recanalized by an intracoronary infusion of urokinase. Coronary cineangiography revealed a total occlusion of the nondominant right coronary artery and no significant narrowing of the left coronary artery. Hemodynamic studies during the acute phase of myocardial infarction demonstrated an increase of right atrial mean pressure in association with normal pulmonary capillary wedge pressure. Following the recanalization, chest pain disappeared and hemodynamic alterations were corrected. The purpose of this report is to document a case of isolated right ventricular infarction due to a nondominant right coronary artery occlusion.     

Acute myocardial infarction with isolated ST-segment elevation in posterior chest leads V7-9: "hidden" ST-segment elevations revealing acute posterior infarction.

OBJECTIVES: This study was done to determine whether electrocardiographic (ECG) isolated ST-segment elevation (ST) in posterior chest leads can establish the diagnosis of acute posterior infarction in patients with ischemic chest pain and to describe the clinical and echocardiographic characteristics of these patients. BACKGROUND: The absence of ST on the standard 12-lead ECG in many patients with acute posterior infarction hampers the early diagnosis of these infarcts and thus may result in inadequate triage and treatment. Although 4% of all acute myocardial infarction (AMI) patients reveal the presence of isolated ST in posterior chest leads, the significance of this finding has not yet been determined. METHODS: We studied 33 consecutive patients with ischemic chest pain suggestive of AMI without ST in the standard ECG who had isolated ST in posterior chest leads V7 through V9. All patients had echocardiographic imaging within 48 h of admission, and 20 patients underwent coronary angiography. RESULTS: Acute myocardial infarction was confirmed enzymatically in all patients and on discharge ECG pathologic Q-waves appeared in leads V7 through V9 in 75% of the patients. On echocardiography, posterior wall-motion abnormality was visible in 97% of the patients, and 69% had evidence of mitral regurgitation (MR), which was moderate or severe in one-third of the patients. Four patients (12%), all with significant MR, had heart failure, and one died from free-wall rupture. The circumflex coronary artery was the infarct related artery in all catheterized patients. CONCLUSIONS: Isolated ST in leads V7 through V9 identify patients with acute posterior wall myocardial infarction. Early identification of those patients is important for adequate triage and treatment of patients with ischemic chest pain without ST on standard 12-lead ECG.     

ST elevation in leads V1 to V4 caused by isolated right ventricular ischemia and infarction

A patient with isolated right ventricular ischemia and infarction is presented. ST elevation in leads V1 to V4 mimicking anteroseptal myocardial infarction was recorded at admission and during episodes of chest pain later on. Noninvasive and invasive workup suggested isolated right ventricular infarction and ischemia due to an occluded small and nondominant right coronary artery.     

Rupture of a giant saccular aneurysm of coronary arteriovenous fistulas

A 58-year-old Japanese woman was admitted to our hospital because of chest pain. A continuous murmur was detected at the left parasternal area. Electrocardiogram showed ST elevation in leads V2, V3 and V4. Chest computed tomography and echocardiography demonstrated pericardial effusion and a large mass which was adjacent to the pulmonary artery. An abnormal blood flow was detected in the mass by Doppler echocardiography. Coronary angiography confirmed that the mass was a giant aneurysm of coronary arteriovenous fistula arising from both the left and right coronary arteries. This patient had no symptoms until rupture of the fistula. Rupture of a coronary arteriovenous fistula is very rare but can be a cause of chest pain and pericardial effusion.     

A pericardial hydatid cyst masquerading as acute inferolateral myocardial infarction--a case report

A case of pericardial hydatid cyst adjacent to the inferoposterial wall of the left ventricle is reported. Significant ST segment elevations in leads D2, D3, aVF, V5, and V6 on surface electrocardiography and sudden onset of severe chest pain mimicked acute inferolateral myocardial infarction. However, cardiac catheterization and coronary angiography showed normal coronary arteries and normal left ventricular cavity. The ST segment elevation in the inferolateral leads disappeared a few days after surgical resection of the cyst. Cardiac hydatid cyst should be considered in the differential diagnosis of patients with angina-like chest pain in endemic areas.     

Multi-arterial myocardial bridge: uncommon clinical and anatomical presentations

We report the case of a 42-year-old man with no risk factors for coronary artery disease admitted with atypical chest pain. The electrocardiogram performed after intravenous injection of nitrate revealed ST-segment elevation in leads V1 to V4. The coronary angiography showed myocardial bridges in the three coronary arteries, besides an unusual length of the left anterior descending artery (80 mm). The patient progressed well following the discontinuation of nitrate use and introduction of beta-blockers and calcium channel antagonists.     

Documentation of early improvement of left ventricular function in tako-tsubo cardiomyopathy

An 86-year-old woman was admitted to our hospital because of chest pain after a heated argument with her daughter. Electrocardiogram showed ST-segment elevation in leads V2-3 and T wave inversion in leads V3-6. Emergency cardiac catheterization was performed 2 h after the onset of chest pain. Coronary angiography showed no significant coronary artery disease. However, left ventriculography showed apical akinesis and basal hyperkinesis (ejection fraction=42%). She was diagnosed as having tako-tsubo cardiomyopathy. Follow-up left ventriculography showed marked improvement of the left ventricular function (ejection fraction=74%) during only 41 h. She was discharged 3 days later.     

Aspiration thrombectomy for acute myocardial infarction resulting from the sequential occlusions of two major coronary arteries in a short time

A 49-year-old man was admitted to our hospital due to chest oppressive sensation. Coronary angiography showed total occlusion in the proximal right coronary artery even after intracoronary nitroglycerin, but no stenosis in the left coronary artery. He was treated with aspiration thrombectomy and stent deployment. After 23 hours, he suddenly had severe chest pain, and ECG showed marked ST elevation in leads I, aVL and V2-6. Surprisingly, coronary angiography showed total occlusion in the proximal left anterior descending artery even after intracoronary nitroglycerin where there had been no stenosis on first angiogram just 23 hours earlier. He was treated with aspiration thrombectomy.     

The ergometrine test: effects on esophageal motility in patients with chest pain and normal coronary arteries

Ergometrine can evoke coronary spasm in patients with variant angina. The cause of ergometrine-induced chest pain in the absence of coronary spasm is not clear. To determine whether ergometrine produced esophageal dysfunction and chest pain, we evaluated 28 patients by esophageal manometry. Six had chest pain in response to ergometrine during cardiac catheterization (group I) and 22 did not (group II). Results of cardiac catheterization were normal in all patients. Seven volunteers with no history of chest pain formed a control group (group III). Esophageal manometry was performed before and after ergometrine administration (0.4 mg I.V.). Ergometrine provocation during esophageal manometry caused significant deterioration in esophageal motility associated with familiar pain in 5/6 group 1 patients. The motility disorders were characterized by repetitive contracts of high amplitude and long duration in the distal esophagus. No patient from group II or III experienced chest pain after ergometrine and only 2 from group II developed long duration contractions. Thus, we conclude that in patients with normal coronary angiograms, ergometrine-induced chest pain without associated coronary spasm suggests that esophageal motility disorders originate chest pain.     

A case of coronary vasospasm treated with stent placement

We report about a 49 year old woman with repeated chest pain at rest. During hyperventilation significant ST-segment elevation in leads V1-V5 appeared. Bicycle stress test did not provoke any ECG changes. Coronary angiography showed a significant stenosis of the left anterior descending coronary artery. Successful balloon angioplasty followed by stent implantation was performed. After an uneventful course of twelve months, hyperventilation could provoke neither chest pain nor ECG changes again without any antispastic medical treatment. Impact of fixed atherosclerotic lesions for the occurrence of coronary vasospasm, usefulness of hyperventilation as a non-invasive provocation test and therapy are discussed.     

Primary angioplasty for infarction due to isolated right ventricular artery occlusion

We report an unusual case of an isolated right ventricular infarction with haemodynamic compromise caused by spontaneous isolated proximal occlusion of the right ventricular branch of the right coronary artery(RCA), successfully treated by balloon angioplasty. A 58-yearold gentleman presented with epigastric pain radiating into both arms. Electrocardiograph with right ventricular leads confirmed ST elevation in V4 R and a diagnosis of isolated right ventricular infarction was made. Urgent primary percutaneous intervention was performed which revealed occlusion of the right ventricular branch of the RCA. During the procedure, the patient’s blood pressure dropped to 80/40 mm Hg, and echocardiography showed impaired right ventricular systolic function. Despite aggressive fluid resuscitation, the patient remained hypotensive, continued to have chest pain and persistent electrocardiograph changes, and hence balloon angioplasty was performed on the proximal right ventricular branch which restored flow to the vessel and revealed a severe ostial stenosis. This was treated with further balloon angioplasty which restored TIMI 3 flow with resolution of patient’s symptoms. Repeat echocardiography showed complete resolution of theST-elevation in leads V4 R and V5 R and partial resolution in V1. Subsequent dobutamine-stress echocardiography at 4 wk showed good left and right ventricular contractions. The patient was discharged after a 3-d inpatient stay without any complications.     

Right ventricular infarction caused by isolated right ventricular branch occlusion: a case report

It is rare to observe right ventricular infarction caused by isolated right ventricular branch occlusion. Isolated right ventricular infarction accounts for less than three percent of all cases of infarction. Generally, it is associated with occlusion of a non dominant right coronary artery or of a right ventricular branch. ECG can be misleading with ST segment elevation in anterior leads. We describe a patient admitted for chest pain with ST segment elevation in leads V1 to V3 associated with ST segment elevation in leads V3R and V4R. Coronary angiography demonstrated isolated total occlusion of the right ventricular branch. Thus, right precordial leads need to be done in every patient presenting with ST segment elevation in precordial leads V1 to V3 and not only in inferior myocardial infarction.     

严重冠脉病变的心电图分析

目的分析左主干、前降支近端或三支病变冠心病心绞痛患者的心电图改变。方法13例冠脉造影诊断为左主干、前降支近端或三支病变的患者,对其静息时、心绞痛发作时心电图有无aVR、V1导联的ST段抬高及临床资料进行分析。结果胸痛发作时11例出现了aVR、V1导联典型改变,静息时2例aVR、V1导联改变。结论心电图aVR、V1导联ST段抬高,尤其STaVR〉STV1,V4～V6导联ST段下移,合并Ⅱ、Ⅲ、aVF导联或Ⅰ、Ⅱ导联ST段下移与冠脉左主干、前降支近端严重狭窄及三支病变有良好的相关性。     

Successful treatment of long spontaneous coronary dissection with medical management: Not to intervene

Spontaneous coronary artery dissection (SCAD) is an uncommon cause of acute coronary syndrome (ACS) and optimal therapy has not been well-defined. We present a case of long SCAD with complete healing due to medical management. A 47-year-old woman presented to emergency department because of sudden onset of typical chest pain. Electrocardiogram (ECG) showed minimal ST-segment elevation in leads V1–V4. Coronary angiography showed a long spiral dissection extending from the middle segment to the distal segment of the left anterior descending artery and TIMI flow grade three. We decided to follow-up with medical management and have control angiography unless hemodynamic instability and chest pain emerged. Control angiography displayed complete healing of dissect segment after six months. SCAD should be considered, especially in women who present with an ACS without a history of cardiovascular disease and risk factor. This report offers the idea that medical management can be a choice even if in the long segment SCAD setting.     

Two cases of primary artery dissection

We experienced two cases of primary coronary artery dissection. (Case 1) 55-year-old man had frequent episodes of chest oppression at early morning and midnight. During chest oppression, electrocardiogram showed transient ST-segment elevation in leads II, III, and a VF. Then, he was diagnosed as having angina pectoris. This diagnosis was based on the fact that he presented coronary spastic syndrome. Right coronary angiogram demonstrated an intimal flap and false lumen at segment 3, and primary coronary dissection was confirmed. (Case 2) A 27-year-old woman complained of back pain while taking a bath. Electrocardiogram showed ST-segment elevation and abnormal Q in leads V2, V3 and V4. She was diagnosed as having acute anterior wall myocardial infarction. Presence of coronary artery dissection at segment 6 was identified by left coronary angiogram. Primary coronary artery dissection is clinically diagnosed by coronary angiogram very rarely. Only 27 such cases have been reported. It was speculated that, in case 1, vasospastic angina may be associated with primary coronary artery dissection. Case 2 had primary coronary artery dissection at segment 6 of the left anterior descending artery. Thus, her clinical picture was similar to those of previously reported cases.     

Pilsicainide-induced coronary vasospasm in a patient with Brugada-type electrocardiogram.

A 65-year-old man with Brugada-type electrocardiogram (ECG) was admitted to our hospital for chest pain, palpitation and faintness. In the cardiac electrophysiological study, no ventricular tachyarrthymia was induced either at baseline or after pilsicainide (50 mg) infusion. Intravenous administration of pilsicainide exaggerated ST-segment elevation in V(1-4) and converted it to the coved type in V(1), accompanied by severe chest pain. Coronary angiography revealed the vasospasm of the right coronary artery was induced by pilsicainide, not by ergonovine. This is the first case report of coronary vasospasm induced by a pure sodium channel blocker in a patient with Brugada-type ECG.     

Unusual ST-t changes in Ebstein's anomaly with occlusion of a nondominant coronary artery

We present a case report of a patient of Ebstein's anomaly presenting with unusual ECG changes during acute coronary syndrome. The patient had undergone radiofrequency ablation of right posteroseptal accessory pathway. Two years later, he presented with acute chest pain. His ECG revealed ST elevation of 6-7 mm in leads III, aVF. V3R and V1-V4 with atrioventricular dissociation. He was thrombolysed for the same. He subsequently underwent an angiogram for continuing angina. His angiogram showed a nondominant right coronary artery with a 95% stenosis. The left circumflex artery was dominant but without any stenosis. The left anterior descending artery was also normal. Angiogplasty and stenting were done for the right coronary artery lesion and the patient did well on follow-up. The ST segment elevation in the anterior precordial leads resulting from occlusion of a nondominant right coronary artery is unusual. The possible reason for this is the isolated right ventricular infarction in the absence of any left ventricular infarction. Thus the electrical current of injury resulting from the right ventricular infarction was unopposed by any counterbalancing current of injury from the inferior surface of the left ventricle.     

Nonsymptomatic myocardial bridge causing systolic total narrowing of circumflex artery

Myocardial bridge is defined as the narrowing of any coronary artery segment in systole but a normal diameter in diastole. It is most frequently seen on left anterior descending (LAD) artery. Left circumflex artery (LCx) is very rare. A 62 year-old male patient presented with severe, squeezing chest pain. The electrocardiogram showed T wave inversion in V1–V4 and ST depression in DII, DIII, aVF. Coronary angiography showed complicated lesion on after S2 branches of LAD and myocardial bridge causing 100% systolic narrowing of fourth obtus marginal branch of LCx. Bare metal stent was placed to LAD lesions with no residual occlusion. The patient was discharged with beta-blocker therapy. He had no recurrent chest pain during six months of follow-up.     

Brugada syndrome unmasked by pneumonia

A 69-year-old white woman presented at our emergency room with right-side pleuritic chest pain, fever, and tachycardia. Results of the physical examination, routine laboratory tests, and chest radiography were unexceptional. An electrocardiogram showed ST elevation in leads V(1) through V(3) with T-wave inversion. Because of the chest pain and the ST elevation, the patient underwent emergency cardiac catheterization, which showed no coronary artery stenosis. A computed tomographic scan of the chest showed pulmonary infiltration in the right middle lobe and the lingula of the left upper lobe; pneumonia was diagnosed, and appropriate antibiotic therapy was started. The electrocardiographic changes met the criteria for type-1 Brugada pattern. Brugada syndrome is an arrhythmogenic disease caused in part by mutations in the cardiac sodium channel gene SCN5A. When the sodium current is disrupted, the outward transient current at the end of phase 1 of the action potential becomes unopposed. This creates a voltage gradient between the epicardium and endocardium, especially in the right ventricular wall, which leads to J-point elevation in leads V(1) through V(3). Fever exaggerates this defect in sodium channels. In our patient, the pleuritic chest pain was caused by the pneumonia, and the ST elevation was probably related to Brugada syndrome, unmasked by the febrile episode. Brugada syndrome can be associated with ventricular tachycardia or fibrillation; the only treatment proven to prevent sudden death is placement of an implantable cardioverter defibrillator, which is recommended in symptomatic patients or in those with ventricular tachycardia induced during electrophysiologic studies.