Andreas Y. Andreou

Split right coronary artery.

1558-2027 2010 Italian Federation of Cardiology (PDA) [1]. Such a RCA divides into an anterior and posterior branch after a single proximal trunk. The anterior branch courses over the free wall of the right ventricle supplying a PDA that courses in the distal posterior interventricular groove to supply the distal posterior interventricular septum. The posterior branch travels in the right atrioventricular groove as the usual RCA extending a PDA that travels in the proximal posterior interventricular groove supplying the proximal (basal) posterior interventricular septum. Split RCA is anatomically the same anomaly as the improperly named ‘double RCA’.

Symptomatic anomalous right coronary artery originating superior to the left aortic sinus with interarterial course in a young adult. Diagnosis with multislice computed tomographic coronary angiography.

Anomalous origination of a coronary artery from the opposite (improper) aortic sinus with interarterial course comprises the group of coronary anomalies with the greatest risk for sudden cardiac death (SCD) in the young. SCD in such settings is consistently related with exercise and driven by ischemia. The proximal ectopic vessel is intussuscepted at the aortic wall and such an anatomy has been documented to be the culprit one. We present a 26-year-old male patient with exercise-induced angina and syncope due to an anomalous right coronary artery, which originated from the tubular ascending aorta superior to the left aortic sinus and followed an interarterial course. Diagnosis was reached with multislice computed tomographic (MSCT) coronary angiography. This case highlights the utility of MSCT to depict the ectopic coronary artery origin and course as

Dual anterior interventricular artery type IV: a rare anatomical variation

Type IV dual anterior interventricular artery (AIVA) is a rare variant that involves bilateral connection of this vessel to the left main coronary artery and right coronary artery or right aortic sinus. We present a case of such a variant where the ectopic branch traveled an intraseptal course, i.e., through the superior aspect of the crista supraventricularis in a subendocardial position and then intramyocardially inside the upper interventricular septum to reach the anterior interventricular sulcus and descend toward the apex. In a left anterior oblique view, this course lacked the typical caudal anterior loop but it was recognized by virtue of emergence of a septal branch as the first branch of the ectopic AIVA. Recognition of this variant and differentiation among the possible courses of the ectopic branch is important for patient management.

A case of crossing coronary arteries.

We present the case of a patient in whom coronary angiography, performed due to severe calcific aortic stenosis, revealed crossing between the left anterior descending artery and the first diagonal branch. There is only a single report presenting this particular coronary anatomy, whereas this is the eleventh case of crossing coronary arteries ever reported. The clinical implications of this variant coronary anatomy with regard to diagnostic angiography and selection of revascularization procedures are briefly discussed.

Dominant right coronary artery occlusion entailing diffuse ST-segment elevation in the precordial leads.

Right ventricular infarction (RVI) during inferior myocardial infarction (MI) is readily diagnosed when ST-segment elevation (STE) is recorded in lead V4R. RVI may also yield precordial STE and such an electrocardiographic (ECG) pattern may be misinterpreted as a sign of anterior MI. We present a case of inferior-right ventricular (RV) MI due to occlusion of a dominant right coronary artery manifesting STE in the inferior, all precordial and right chest leads. RV dilation due to acute ischemic insult facilitated STE in leads V1-V4 despite the dominant opponent inferior and posterolateral left ventricular injury current. This case illustrates that dilation of an infarcted RV should be considered when such an ECG pattern is encountered during inferior MI, specifically a dominant one. Awareness of the circumstances under which this ECG pattern develops facilitates avoidance of misinterpretation as a sign of anterior MI and proper management.

Optical coherence tomography: the face of coronary artery spasm.

diabeticpatientswith acuteheart failurewas increased compared tonondiabetics. Among diabetics 7.3% required levosimendan and 15% underwent percutaneous coronary intervention because of acute coronary syndrome. Data concerning the hypoglycemic treatment of those patients was not collected. Should this missing information be provided, the potential implication of SUs in counteracting levosimendan and blocking the preconditioning phenomenon could be further evaluated. The authors of this manuscript have certified that they comply with the principles of ethical publishing in the International Journal of Cardiology [15].

Preinfarction angina entailing precordial ST segment depression with positive T wave.

To the Editor A 46-year-old male, cigarette smoker with dyslipidemia was admitted because of atypical chest pain associated with nonspecific T wave abnormalities in leads III and aVF. Serial cardiac enzyme evaluation, including troponin, was negative and he was discharged home following absence of exercise-induced ischemia. Three days later, he was readmitted because of acute rest angina. His ECG recorded during pain displayed a heart rate (HR) of 68 beats/min, ST segment depression (STD) with positive and peaked T waves in leads I, II, aVL and V2–V6 and absence of ST segment elevation (STE) in the posterior leads (Fig. 1a). Medical therapy resulted in abolishment of angina and STD resolution, but inverted T waves in leads III and aVF. About 1 h later, angina recurred in association with STD and peaked positive T waves in leads V2–V6, loss of R wave in V2, a Q wave in V3, subtle STE in lead III, pseudonormalization of the T wave in aVF and STD in I and aVL (Fig. 1b). Echocardiography during this phase displayed left anterior descending artery (LADA)-related segmental akinesia. Angina continued despite maximally tolerated medical therapy and provided the acute ischemic ECG changes, we recommended urgent coronary angiography. However, the patient expressed his preference to have this examination done in a private hospital, thus immediate transfer was arranged. Unfortunately, a precatheterization ECG was not performed, but provided that the angiogram displayed a total proximal LADA occlusion (Fig. 2) without collateral flow, we presumed that the ECG showed an STE pattern. The left circumflex (LCx) artery contained an intermediate proximal stenosis, whereas the dominant right coronary artery (RCA) was free of atherosclerosis (Fig. 2). The LADA was successfully tackled with a sirolimus-eluting stent. Creatine kinase and creatine kinase-myocardial band isoenzyme

Stenting for an internal mammary artery graft kink

MOTS CLÉS Pontage mammaire interne ; Greffon coronaire A 60-year-old male cigarette smoker with hypertension and hyperlipidaemia underwent coronary artery bypass surgery after hospitalization for unstable angina. An in situ, pedicled, left internal mammary artery (LIMA) was grafted to the left anterior descending (LAD) artery, and vein grafts were placed to the right posterior descending and obtuse marginal arteries. One month later, the patient underwent repeat angiography for severe angina; this revealed patent vein grafts and a significant LIMA stenosis at the site of a kink (Fig. 1), which was refractory to selective catheter injection of nitroglycerine. Because no other possible culprit lesion was revealed, we intervened directly with deployment of a 3.0 mm × 15 mm everolimus-eluting stent across the kink site. This led to complete resolution of the stenosis; sustained relief of angina was confirmed at 1-year follow-up. Kinking of an IMA graft is a rare cause of significant stenosis and recurrent ischaemia. It is produced secondary to distortion of the geometry of the graft either due to stretching of the naturally tortuous IMA to facilitate grafting or looping of a redundant graft induced by inadvertent twisting. Kinking may be intermittent and produced secondary to marked bending of a redundant graft induced by lung motion. Both pedicled and skeletonized IMAs develop kinks with similar frequencies; however, the associated stenosis severity is significantly higher in the latter, possibly due to the small amount of connective tissue left around the graft to serve as a cushion that facilitates kink development at a sharper angle. Furthermore, documented cases of spontaneous resolution of such kinks have implicated local wall oedema and haematoma produced during harvest as possible causes of IMA graft kinking. Perioperative IMA spasm may simulate a kink and although it may be intractable, its resolution after intraconduit administration of vasodilators facilitates their differentiation.

Right posterior sinoatrial node artery showing a pericaval course: a previously undescribed mode of termination

The left posterior sinus node artery (PSNA) originates from the posterolateral left circumflex artery, is quite common and shows more frequently a retrocaval mode of termination. In contrast, the right PSNA that arises from the terminal right coronary artery has been rarely described while information on its mode of termination is generally lacking. The PSNA courses close to the ostia of the superior pulmonary veins; hence, it may get injured during surgical or catheter ablation procedures performed for the treatment of atrial fibrillation. The left PSNA terminates retrocavally more frequently than the usual SNAs; hence, it may be at a greater risk of transection during the popular superior septal approach to the mitral valve. We present a case of right PSNA which terminated in a previously unreported course, i.e., the pericaval. Discussion pertains to the anatomic features of the PSNA that render it susceptible to the aforementioned complications.

Coronary Extramural Haematoma Caused by Perforation during Left Main Coronary Artery Intervention

A year-old male patient with a background of quintuple coronary artery by-pass graft surgery 16 years ago presented to our department with symptoms consistent with unstable angina pectoris. Previous angiography performed in 2001 revealed occluded saphenous vein grafts to the left anterior descending (LAD), right coronary, obtuse The presence of pericardial effusion was immediately ruled out by echocardiography and because of absence of myocardial contrast staining heparin was not reversed. Subsequent intravascular ultrasound (IVUS) examination revealed a minimal lumen area of ≥11.00 mm2 throughout the stented segment despite stent underexpansion at marginal and first diagonal (DA) arteries, and patent left internal mammary artery (LIMA) graft to a second DA. At the same session he underwent percutaneous coronary intervention with bare metal stent implantation for significant mid to distal LAD artery disease. Since then, the patient was stable with Canadian angina class I. During this admission, his echocardiogram revealed an ejection fraction of 40%, akinesia of the inferior wall which was known to be predominantly infarcted and hypokinesia of the basal and mid anterior septum. Coronary angiography (Fig. 1) showed subocclusive calcified and angulated distal left main coronary artery (LMCA) disease, significant ostial LAD artery disease, collateralised occlusion of the distal LAD, left circumflex (LCx) and right coronary arteries, tight proximal disease of a first DA and patent LIMA graft to a second DA. Given these findings we proceeded with stent angioplasty to the LMCA-ostial LAD artery lesion. After a series of predilations with semicompliant balloons, a 4.0 mm × 24 mm drug-eluting stent was the LMCA opposite to the LCx artery ostium and at the LAD artery ostium. Cross-sections of IVUS at the site of perforation revealed an echo-dim pattern suggesting an extramural haematoma and local stent underexpansion with a compression effect by the haematoma whereas the site of blood entry into the adventitia was identified at the distal margin of the haematoma adjacent to a fibrocalcific plaque (Fig. 2). Given the adequate minimal lumen area further stent postdilation was not performed to avoid the risk of frank coronary perforation. The patient was maintained on dual antiplatelet therapy and discharged home after a two-day uneventful hospital course. He remained stable eight months post stenting with Canadian angina class I and no evidence of a cardiovascular event. Extramural haematoma that is accumulation of blood outside the arterial wall in the adventitia tissue is a rare complication of percutaneous coronary intervention and is thought to develop secondary to adventitial dissection implanted from the ostium of the LMCA across the stenosis into the LAD artery at 8 atms. Control angiography after [1–3]. It presents with an echo-dim pattern due to the dilution of the red blood cells and dissemination throughout