Coronary Rupture Research Articles

A Case of Arterial and Venous Tear during Single Lead Extraction.

Transcutaneous lead extraction can be associated with significant morbidity and mortality. The risk of causing concomitant arterial and venous injury is rare. We report a case of marginal artery rupture with coronary sinus rupture after a CS lead extraction. A 71-year-old male was admitted for extraction of a 6-year-old implantable cardioverter-defibrillator lead due to fracture from insulation break. During the lead extraction, blood pressure fell precipitously and echocardiographic findings were consistent with pericardial effusion. After unsuccessful pericardiocentesis, open chest sternotomy and evacuation of hematoma was performed. Subsequent surgical repair of several injuries was completed including the distal coronary sinus, a large degloving injury of posterior portion of the heart, and first obtuse marginal branch bleed. This case demonstrates that when performing transcutaneous lead extraction (TLE) with laser sheath, a degloving injury can cause arterial rupture with concomitant coronary sinus injury. A multidisciplinary team-based approach can ensure patient safety. Learning Objective. Implantable cardioverter-defibrillator leads will falter over time. With the advancement of new technology for extraction more frequent and serious complications will occur. Active fixation CS leads present unique challenges. In the presence of hemodynamic changes during extraction the occurrence of both an arterial and venous injury must be considered.

Acute coronary syndromes

Acute coronary syndromes

Abstract 20008: Echoing Plaque Activity of Coronary Artery With Intracranial Artery in Acute Ischemic Stroke Patients: Coronary CT Angiography and High-resolution MR Imaging Study

Background: Atherosclerosis is a systemic disease, and both coronary and intracranial atherosclerosis are common in elderly. Unlikely to coronary artery disease (CAD), intracranial atherosclerotic disease (ICAD) can cause stroke by branch occlusive disease-type (B-type ICAS), subcortical infarcts caused by parent arterial disease occluding perforator’s orifice as well as coronary type rupture of plaque (C-type ICAS).Vascular pathophysiology of coronary atherosclerosis in relationship with different phenotypes of intracranial atherosclerosis is unknown. Methods: We prospectively recruited 69 patients with acute cerebral infarcts caused by ICAS who had no history of CAD. Patients underwent both cardiac multidetector computed tomography (MDTC) and brain high-resolution MRI (HR-MRI). Symptomatic steno-occlusive intracranial artery at the maximal stenosis on MRA was analyzed in terms of vascular morphology (stenosis degree, remodeling index, and wall index) and activation (enhancement pattern and volume) using HR-MRI. Asymptomatic CAD burden (number and degree of stenosis) and plaque characteristics (calcified, mixed, and non-calcified) were measured with MDCT. The degree of asymptomatic ICAD was also measured in each patient (number of stenotic arteries and degree of stenosis). Results: The mean age of the patients were 65.1±1.5 years, 59.4% were male, and 35 (51.7%) were diagnosed with C-type ICAS. Asymptomatic CAD was observed in most patients, and increase in CAD burden was associated with increased asymptomatic ICAD (p<0.01). Overall CAD burden were not different between B-type and C-type ICAS. However, prevalence of non-calcified coronary plaque were much higher in C-type ICAS (35.3% vs 62.9%, p=0.02). C-type ICAS group also showed higher degree of stenosis (40.4 ±34.5 vs 77.3±17.3, p<0.001), increased positive remodeling index (1.0±0.3 vs 1.3±0.5, p=0.03), and larger proportion of vessels with enhancement (73.5% vs 97.1%, p<0.01) in cerebral arteries compared to B-type ICAS. Conclusions: Plaque characteristics of intracranial and coronary behave in same way. Further studies are needed to find systemic factors associated both intracranial and coronary plaque progression.

Abstract O.59: Fate of Kawasaki disease giant coronary aneurysm: Analysis of the last 10 years nationwide survey in Japan

Background and Objective: Long term prognosis of Kawasaki disease (KD) with giant aneurysm is not yet well understood. We conducted a nationwide survey of KD with giant aneurysm for recent 10 years, and analyzed cardiac events of those patients. Methods: Nationwide epidemiological survey of KD has been conducted every 2 years since 1970 in Japan. We performed questionnaire survey based on 16th - 21th (1999 - 2010) nationwide epidemiological data. Results: We send questioners to 275 facilities asking about 415 patients who were reported to have giant aneurysm (>=8mm), and collected the data of 334 patients (80.5%). We excluded 84 non-giant aneurysm patients and 36 duplicated cases and difined finally 214 patients. Out of 214 patients, 13 deaths and 32 AMIs were described (6.1% and 15.0%, respectively). The first AMI attack was mostly reported within a few months from KD onset (medium 5 months (0-85 months)). AMI was occurred one time in 26 patients, and two times in 6 cases. Myocardial ischemia was observed in 80% of AMI patients, and 12 patients were received coronary artery bypass graft. Thirteen patients were reported to be dead (medium 1 month (0-23 months) from KD onset). There were 6 cardiac deaths within 1 month from KD onset (5: rupture of aneurysm, 1: AMI). The others were all caused by AMI except for 2 accidental death. Four out of 6 AMI deaths were caused by the first AMI attack. For the remaining 2 AMI deaths, the period from the first AMI to second fatal AMI was 1 month and 6 month, respectively. There were no death reported byond 2 years from KD onset. Conclusion: AMI and cardiac death of KD with giant aneurysm occurred mostly in early phase of KD onset. Coronary rupture occurs within a month after onset, and 84% AMI and all AMI death occurs within 2 years after onset. Patients survival become promising after 2 years from onset. These evidences indicate that therapeutic strategy up to 2 years after onset is extremely important for prognosis of KD with giant aneurysm.

Elective percutaneous coronary intervention complicated by coronary rupture

Elective percutaneous coronary intervention complicated by coronary rupture

Elective percutaneous coronary intervention complicated by coronary rupture

Elective percutaneous coronary intervention complicated by coronary rupture

Avoiding Coronary Occlusion and Root Rupture in TAVI - The Role of Pre-procedural Imaging and Prosthesis Selection.

Coronary occlusion and rupture of the aortic root or annulus remain two major concerns of transcatheter aortic valve implantation technique. Despite their relatively low frequency they raised the interest of the scientific community as they carry an extremely poor prognosis. Prosthesis type and size selection is part of the patient selection process that allows the operator to prevent these complications. In this article, the techniques used either during pre-TAVI screening or during the procedure itself to avoid coronary occlusion and aortic rupture will be discussed.

A Lifesaving Abdominal Pain: Unusual Presentation of Giant Coronary Artery Aneurysm among Multiple Aneurismatic Coronary Disease

Coronary artery aneurysms are rare with a prevalence estimated between 0.3-5% among people undergoing angiography. Giant coronary artery aneurysms (CAA) defined as having a diameter of 2 cm or greater are rare with a reported prevalence of 0.02%. Combination of giant coronary aneurysm with multiple fusiform aneurysms in the remaining coronary arteries is even rarer. Giant CAAs are prevalent in adult male and predominant in right coronary artery; the etiology is atherosclerotic or associated with Kawasaki disease, Takayasu arteritis, collagen vascular disease, IgG4-related coronary periarteritis or secondary to drug-eluating stent implantation. Complications could be thrombosis of the aneurismal sac with secondary acute coronary syndrome or rupture of the sac with fatal consequences, but patients can be completely asymptomatic. We describe an interesting case of a 58 year-old man who had multiple atherosclerotic CAA, one of which was a giant CAA of the right coronary artery presenting to us claiming abdominal pain without any kind of cardiac symptoms.

Abstract 88: Blockade of ETS-1 Attenuates EGF-Induced Collagen Loss in Carotid Plaques of Patients With Carotid Stenosis

Introduction: Coronary thrombosis and rupture of plaques leading to stroke are major causes of morbidity and mortality. Here, we examined the role of v-ets erythroblastosis virus E26 oncogene homologue-1 (ETS-1) on the epidermal growth factor (EGF)-induced destabilization of collagen type I (Col-Iα1) and collagen type III (Col-IIIα1) involving matrix metalloproteinase-1 (MMP-1) and MMP-9 in isolated vascular smooth muscle cells (VSMCs) from the plaques of symptomatic (S) and asymptomatic (AS) patients with carotid stenosis. To understand the molecular mechanisms underlying EGFR-regulated ETS-1, the signaling pathways directing ETS-1 production was investigated and examined if EGF-induced loss of fibrillar collagens in patients with carotid stenosis is regulated by ETS-1. Methods: VSMCs isolated from carotid plaques of both AS and S patients were treated with or without EGF. The mRNA transcripts and protein for ETS-1, MMP-9 and -1, EGFR, Col-I(α1) and Col-III(α1) were analyzed by qPCR and immunofluorescence, respectively. Results: Treatment of VSMCs with EGF significantly increased ETS-1 expression and immunoreactivity in S compared to AS. EGFR inhibitor (AG1478) decreased ETS-1 expression and upregulated Col-I(α1) and Col-III(α1) in EGF-treated VSMCs of both groups. In the transfection experiments, overexpression of ETS-1 in VSMCs increased mRNA transcripts of MMP-9 and MMP-1 and decreased the collagen mRNA transcripts. Knock-down of ETS-1 gene with either siRNA or transfection with dominant-negative form (ETS-DN) blocked EGF-induced MMP-1 and MMP-9 expression and increased mRNA transcripts for Col-I(α1) and Col-III(α1) in S compared to AS group. Inhibitors of p38MAPK (SB202190) and JNK-II (SP600125) decreased ETS-1, MMP-1 and MMP-9 transcripts and increased collagen transcripts in EGF-treated VSMCs, suggesting that p38MAPK and JNK pathways are involved in EGFR-induced collagen loss. Conclusion: These findings revealed a novel mechanism of ETS-1-regulated EGF-induced collagen loss in human carotid plaques and this could be a leading cause of plaque instability in patients with carotid stenosis. Selective blockade of ETS-1 and EGFR may be novel strategy and promising target for treating unstable and vulnerable plaques.

PP-256 Coronary Fistula between Left Anterior Descending (LAD) Arter to a cavity in Right Ventricule with Proximal LAD Lesion and Succesfully Treatment with Coil Embolisation and Coronary Stenting

Introduction: Coronary artery fistulas ( CAF) are rare, abnormal communications between coronary arterial bed and cardiac chambers or pulmonary circulation. Frequency have been reported as 0.05-0.25 % in coronary angiographic studies. Theraphy could be surgery, percutan closure with coil embolisation or occluder device, conservative management depend on fistul diameter and shunt flow. Mostly right coronary artery fistulate to right heart chambers or pulmonary artery. Fistulisation of LAD to a cavity in right ventricule is very rare. We introduce a a patient in this clinical condition with proximal LAD lesion that treated with coil embolisation and coronary stenting. Case: A 46 year old man appealed to our clinic cause of efor angina. In his echocardiogram a cavity was seen in right ventricule close to septumapical region ( Figure 1A). A coronary angiogram was done since his treadmill test positive. In his coronary angiogram LAD was aneurismatic, there was severe stenosis in proximal part of LAD ( Figure 1B, Video 1). Also LAD was continuing to apex and spilling a cavity suggested in right ventricule that was seen in echocardiogram (Figure 1C, Video 1). Cardiac computed tomography (CT) angiogram was confirmed that anatomy(Figure 1E,1F,1G). A decission was made to percutaneous intervention to LAD lesion and coil embolisation to fistul instead of surgery. Fistula was occluded succesfully with coil embolisation first (Figure 1D, Video 1), than stenting of proximal LAD was proceeded (Figure 1H, Video 1). Patient was discharged after two days uneventful following. Discussion: Treatment of CAF is challenging since large amount of variation an lack of guideline based treatment suggestions. Small fistulas which do not cause any symptom, heart chamber enlargment, pulmonary hypertension or cardiac ischemia could be followed medically. Large fistulas requires invasive treatment as surgery or percutaneous coronary intervention (PCI). PCI could be done with coil embolisation or amplatzer occlusion devices. Ligation of fistula with surgery in aneurismatic coronary arteries carries risk of coronary rupture. In our patient there was a severe narrowing at proximal part of LAD. We prefere PCI rather than one vessel by pass graft and fistula ligation surgery since LAD flow would diminish after ligation of fistula and that could impair negatively to graft functions. PCI has provided more physiologic coronary flow and succesful result.

Successful management of Ellis type III left anterior descending artery perforation following percutaneous coronary intervention by a covered stent: Successfully resolved the dramatic complication

Coronary artery perforation is a rare but catastrophic complication of percutaneous coronary intervention (PCI). Grade III coronary perforation and rupture invariably results in pericardial effusion and tamponade requiring urgent pericardiocentesis. Advances in coronary intervention have increased the opportunity to treat coronary artery perforation. We are reporting a case of 55 years old hypertensive female who presented with effort angina. Coronary angiogram revealed significant stenosis in the left anterior descending coronary artery. Post PCI, she had Ellis type III coronary perforation and pericardial tamponade and cardiogenic shock. The patient was resuscitated, pericardiocentesis done, autologous blood transfusion given and covered stent deployed.

Two Cases of Super-Giant Coronary Aneurysms after Kawasaki Disease

Acute giant coronary aneurysm after Kawasaki disease (KD) is a catastrophic complication that can be fatal and very difficult to manage. However, no fixed consensus has been reached for the management of super-giant coronary aneurysms in the acute setting. Here, we report the successful management of young children with super-giant coronary aneurysms after KD. Based on our experience, hemodynamic stabilization to prevent further coronary dilation or rupture and strict anticoagulation to avoid thrombus formation are mandatory in the management of this condition.

Sick Sinus Syndrome Induced by Giant Coronary Artery Aneurysm Rupture in a Patient with Constrictive Pericarditis

Multiple coronary artery aneurysms (CAA) with a giant CAA are rare. Patient with a giant CAA is at risk of thrombosis, aneurysm rupture and even sudden cardiac death. We reported a case of a 78-year-old woman having a giant CAA (43 mm × 37 mm) of proximal left anterior descending artery as well as multiple small CAA of both left and right coronary arteries. The spontaneous rupture of the giant CAA combined with previously undiagnosed constrictive pericarditis leaded to severe dyspnea, edema of lower extremities, and syncope. Emergency electrocardiogram (ECG) showed remarkable sinus bradycardia, sinus arrest and atrioventricular junctional rhythm, indicating sick sinus syndrome. Temporary cardiac pacemaker therapy was performed urgently to avoid sudden cardiac death. Multiple non-invasive imaging tests revealed constrictive pericarditis possibly caused by tuberculosis, and giant CAA with the possibility of rupture. Then pericardiotomy and resection of giant aneurysm were performed urgently. Postoperative course was uneventful. The patient became asymptomatic and was discharged in good health. To the best of our knowledge, this is the first case of spontaneous rupture of giant CAA in a patient with constrictive pericarditis, with a rare complication of sick sinus syndrome.

Dysfunctional nitric oxide signalling increases risk of myocardial infarction

Myocardial infarction, a leading cause of death in the Western world, usually occurs when the fibrous cap overlying an atherosclerotic plaque in a coronary artery ruptures. The resulting exposure of blood to the atherosclerotic material then triggers thrombus formation, which occludes the artery. The importance of genetic predisposition to coronary artery disease and myocardial infarction is best documented by the predictive value of a positive family history. Next-generation sequencing in families with several affected individuals has revolutionized mutation identification. Here we report the segregation of two private, heterozygous mutations in two functionally related genes, GUCY1A3 (p.Leu163Phefs*24) and CCT7 (p.Ser525Leu), in an extended myocardial infarction family. GUCY1A3 encodes the α1 subunit of soluble guanylyl cyclase (α1-sGC), and CCT7 encodes CCTη, a member of the tailless complex polypeptide 1 ring complex, which, among other functions, stabilizes soluble guanylyl cyclase. After stimulation with nitric oxide, soluble guanylyl cyclase generates cGMP, which induces vasodilation and inhibits platelet activation. We demonstrate in vitro that mutations in both GUCY1A3 and CCT7 severely reduce α1-sGC as well as β1-sGC protein content, and impair soluble guanylyl cyclase activity. Moreover, platelets from digenic mutation carriers contained less soluble guanylyl cyclase protein and consequently displayed reduced nitric-oxide-induced cGMP formation. Mice deficient in α1-sGC protein displayed accelerated thrombus formation in the microcirculation after local trauma. Starting with a severely affected family, we have identified a link between impaired soluble-guanylyl-cyclase-dependent nitric oxide signalling and myocardial infarction risk, possibly through accelerated thrombus formation. Reversing this defect may provide a new therapeutic target for reducing the risk of myocardial infarction.

Interpretation of mild elevation of high-sensitivity cardiac troponins

Measurements of cardiac troponins (cTn) are yet considered the gold standard method in patients with chest pain. Very recently, high-sensitivity (hs)cTn emerged and allow to measure very low concentrations of cTn. The aim of these assays was the better detection of patients with acute myocardial infarction (AMI). The threshold value should be the 99th percentile of the method, which corresponds to the concentration obtained from 99% of a reference population. These assays improve the detection of patients with elevated cTn concentrations. All patients with increased hs-cTn concentration above the 99th percentile should be considered at high risk of future clinical event when compared to patients with lower concentration. However, these elevated concentrations are not necessarily related to AMI due to coronary artery plaque rupture and superimposed thrombus. In order to understand adequately cTn measurement, the physician should base his interpretation on the context, the cTn concentration, variations during serial sampling, and the possible existence of a coexistent disease characterized by increased cTn concentrations.

A Coronary Rupture in the Left Anterior Descending Artery at Second Diagonal Artery Bifurcation Level in an Intervention with a Tryton Side Branch Stent

Percutaneous coronary intervention (PCI) for bifurcation lesions (BLs) is considered high risk due to increased procedural adverse events when compared to non-bifurcation lesion. Dedicated bifurcation stents, specifically designed to allow minimally traumatic implantation in the main vessel and/or side branch while providing adequate scaffolding of the side branch ostium may offer an advantage over utilization of conventional stents. Coronary perforation as a complication of PCI is a rare but potentially lethal complication that is associated with a high rate of morbidity. Coronary artery perforation during PCI has been reported repeatedly. To our best knowledge perforation in a BL, PCI with the Tryton Side-Branch Stent has not been reported. This case highlights that the Tryton to be an easy-to-use device in BLs, also operator should be careful, not too aggressive, their potential risks should be born in mind and a graft stent must be available in catheterization laboratory for emergencies.

Tratamento de perfuração coronária tipo IV durante intervenção coronária percutânea

Relatamos o caso de um paciente de 61 anos de idade, hospitalizado por angina instável. Cineangiocoronariografia demonstrou lesão obstrutiva grave no terço médio da artéria descendente anterior. Intervenção coronária percutânea foi realizada com implante de stent. Logo depois da pós-dilatação com cateter-balão, observou-se ruptura coronária, com extravasamento de contraste para o ventrículo esquerdo (perfuração coronária tipo IV). Após reversão parcial da heparina com protamina e insuflação prolongada do cateter-balão com baixa pressão, a ruptura coronária foi controlada, com bom resultado angiográfico final. Ecocardiografia realizada em seguida evidenciou derrame pericárdico mínimo. A evolução clínica foi satisfatória após o procedimento.

Treatment for Type IV Coronary Perforation during Percutaneous Coronary Intervention

We report the case of a 61-year-od male, hospitalized for unstable angina. Coronary angiography showed a severe lesion in the middle third of the left anterior descending coronary artery. Percutaneous coronary intervention was performed with stent implantation. Coronary rupture was observed with contrast spilling to the left ventricle (type IV coronary perforation) immediately after balloon post-dilatation. After partial heparin reversal with protamine and prolonged balloon inflation at low pressure, coronary rupture was controlled, with a good final angiographic result. Subsequent echocardiography showed minimal pericardial effusion. Post-procedure clinical follow-up was satisfactory. Tratamento de Perfuração Coronária Tipo IV Durante Intervenção Coronária Percutânea Relatamos o caso de um paciente de 61 anos de idade, hospitalizado por angina instável. Cineangiocoronariografia demonstrou lesão obstrutiva grave no terço médio da artèria descendente anterior. Intervenção coronária percutânea foi realizada com implante de stent. Logo depois da pós-dilatação com cateter-balão, observou-se ruptura coronária, com extravasamento de contraste para o ventrículo esquerdo (perfuração coronária tipo IV). Após reversão parcial da heparina com protamina e insuflação prolongada do cateter-balã com baixa pressao, a ruptura coronária foi controlada, com bom resultado angiográfico final. Ecocardiografia realizada em seguida evidenciou derrame pericárdico mínimo. A evolução clínica foi satisfatória após o procedimento.

Allergic myocardial infarction

Allergic myocardial infarction

The Human Knee: Gross, Microscopic, Surgical, and Radiological Anatomy

The Human Knee: Gross, Microscopic, Surgical, and Radiological Anatomy