Lateral Infarction Research Articles

Resección de aneurisma de arteria esplénica por vía laparoscópica conservando el bazo

Laparoscopic surgical excision of a splenic aneurism Elective surgical repair is indicated for splenic aneurisms when they are wider than 20 mm, during pregnancy and when a progressive increase in diameter is documented. We report a 63 years old female with a history of hypertension, presenting with pain in the right upper quadrant. An abdominal CAT scan disclosed a hepatic cyst and an aneurism of the splenic artery of 20 mm diameter. A laparoscopic excision of the aneurism was carried out without performing a splenectomy. A CAT scan done one month later postoperative period detected a small lateral spleen infarction and a subcapsular collection of 2 cm diameter.

Isolated lateral thalamic infarction: the role of posterior cerebral artery disease

Lateral thalamic infarction (LTI) is usually caused by small vessel disease (SVD), i.e., occlusion of the deep perforator. However, focal atherosclerotic posterior cerebral artery disease (PCAD) may produce LTI via thrombotic occlusion of the perforator. We aimed to investigate the prevalence of PCAD in LTI and differences in clinical and imaging findings between LTIs associated with PCAD and SVD. We retrospectively evaluated 58 consecutive patients with isolated LTI who underwent diffusion-weighted imaging (DWI) and MR angiography (MRA) within 7 days after stroke onset. Patients were divided into two groups: those with PCAD and those with SVD. Clinical syndromes were divided into pure sensory stroke (PSS) and sensory stroke plus (SS-plus), i.e., the concomitant presence of motor dysfunction or ataxia. Clinical and imaging findings were compared between these two groups. Of the 58 patients, 13 (22.4%) had PCAD. PSS was more frequently associated with SVD than with PCAD (57.8% vs. 23.1%, P=0.032). Initial DWI lesion volume (cm³) was significantly larger in PCAD than in patients with SVD (0.38±0.13 vs. 0.33±0.22, P=0.025). Among the 23 patients (39.7%) who underwent follow-up DWI, patients with PCAD showed a significantly greater increase in subacute lesion volume than those with SVD (P=0.019). Although National Institutes of Health Stroke Scale scores did not differ at admission (P=0.185), they were significantly higher at discharge in PCAD than in patients with SVD (P=0.012). Our data suggest that PCAD is an important cause of LTI, being related to SS-plus, larger lesion volume, and worse clinical outcomes.

Connective Tissue Growth Factor and the Parallels Between Brain Injury and Brain Tumors

JNCI | Editorials 1141 Glioblastoma is the most common primary brain tumor, comprising 52% of all primary brain tumors. Despite advances in treatment, glioblastoma remains virtually incurable, with a median survival of approximately 15 months. A chief cause of the high mortality of glioblastoma is the invasive nature of the tumor, which renders full resection of tumor cells practically impossible. Thus, understanding the mechanisms that underlie glioblastoma invasion is crucial for developing new treatment approaches for this devastating disease. In this issue of the Journal, Edwards et al. (1) identify connective tissue growth factor (CTGF) as a secreted factor that stimulates the migration and invasion of glioblastoma cells. They show that CTGF, which is produced at high levels by reactive astrocytes bordering the tumor, binds a complex comprising tyrosine kinase receptor type A (TrkA) and integrin B1 on glioma cells, which leads to the activation of nuclear factor kappa B (NF-kB) signaling. NF-kB signaling activates the zinc finger E-box-binding homeobox 1 (ZEB-1) transcription factor, which transcriptionally represses E-cadherin, thereby enhancing invasion and migration. CTGF is a potent modulator of intercellular signaling and extracellular matrix function. It has chemotactic and mitogenic activity for fibroblasts and other cells. CTGF expression is induced by many growth factors, and CTGF itself binds directly to bone morphogenetic proteins, transforming growth factor B, and vascular endothelial growth factor (VEGF) and modulates their activities. It stimulates the production of extracellular matrix components such as collagen and fibronectin as well as integrins. CTGF also binds integrins and various matrix components, including heparin, fibronectin, and matrix metalloproteinases, and this binding alters the activities of both extracellular matrix components and CTGF itself (2,3). CTGF expression is most frequently linked to pathologies associated with inflammation and fibrosis throughout the body. For example, CTGF expression has been implicated in fibrosis of the kidney, liver, lung, pancreas, and skin; in atherosclerosis; and in inflammatory bowel syndromes. Strikingly, CTGF is overexpressed in many cancers that have a substantial fibrotic component, including pancreatic cancer, breast cancer, and melanoma. CTGF expression is also high in sarcomas and chondrosarcomas, which like fibroblasts are of the mesodermal lineage (3,4). In the brain, elevated CTGF expression has been observed in various cell types, primarily during injury response, inflammation, and reactive gliosis. For example, increased CTGF expression is seen in spinal cord injury, amyotrophic lateral sclerosis, cerebral infarction, brain trauma, and models of excitotoxic brain damage (5,6). Elevated expression of CTGF is well characterized in reactive astrocytes, and CTGF is also expressed in pathological contexts by microglia, fibroblasts, smooth muscle cells, endothelial cells, and neurons (5,7). Not surprisingly, then, altered CTGF expression has been observed in brain tumors as well. Indeed, CTGF is overexpressed in 58% of primary gliomas, and expression is correlated with tumor grade and patient survival independent Connective Tissue Growth Factor and the Parallels Between Brain Injury and Brain Tumors

Bilateral Orbital Bone Infarction in Sickle-Cell Disease

This is a case of a 2-year-old boy with sickle cell disease who presented with bilateral eyelid swelling, limited extraocular motility, and lateral subperiosteal fluid collection associated with bilateral lateral orbital wall infarctions on MRI. The patient was managed medically with intravenous fluids, analgesics, broad-spectrum antibiotics, systemic steroids, and clinically improved. Patients with sickle cell disease are susceptible to infarction of the orbital bones during vaso-occlusive crises. Orbital wall infarction can lead to acute proptosis and restricted extraocular motility. Orbital wall infarction should be considered in sickle cell patients with orbital diseases so that appropriate treatment can be instituted promptly to prevent the serious sequelae of orbital compression syndrome.

Administration of Pigment Epithelium-Derived Factor Inhibits Left Ventricular Remodeling and Improves Cardiac Function in Rats with Acute Myocardial Infarction

Oxidative stress and inflammation are involved in cardiac remodeling after acute myocardial infarction (AMI). We have found that pigment epithelium-derived factor (PEDF) inhibits vascular inflammation through its anti-oxidative properties. However, effects of PEDF on cardiac remodeling after AMI remain unknown. We investigated whether PEDF could inhibit left ventricular remodeling and improve cardiac function in rats with AMI. AMI was induced in 8-week-old Sprague-Dawley rats by ligation of the left ascending coronary artery. Rats were treated intravenously with vehicle or 10 μg PEDF/100 g b.wt. every day for up to 2 weeks after AMI. Each rat was followed until 16 weeks of age. PEDF levels in infarcted areas and serum were significantly decreased at 1 week after AMI and remained low during the observational periods. PEDF administration inhibited apoptotic cell death and oxidative stress generation around the infarcted areas at 2 and 8 weeks after AMI. Further, PEDF injection suppressed cardiac fibrosis by reducing transforming growth factor-β and type III collagen expression, improved left ventricular ejection fraction, ameliorated diastolic dysfunction, and inhibited the increase in left ventricular mass index at 8 weeks after AMI. The present study demonstrated that PEDF could inhibit tissue remodeling and improve cardiac function in AMI rats. Substitution of PEDF may be a novel therapeutic strategy for cardiac remodeling after AMI.

Interpretation of Annular Tissue Doppler Imaging

Refer to the page 137-142 Diastolic dysfunction has become a more predominant form of heart failure (HF) than systolic dysfunction in the community. However, diastolic dysfunction is not always related to HF. Diastolic HF is defined as HF with preserved left ventricular (LV) systolic function, usually a LV ejection fraction (EF) of more than 50%, in the absence of valvular heart disease. The clinical importance of diastolic dysfunction has increased because its prevalence has increased with worsening morbidity and mortality, especially in the elderly and women. The standard criteria for LV diastolic dysfunction is characterized by impairment of LV relaxation during the isovolumic relaxation time (Tau) in cardiac catheterization. However, routine invasive cardiac catheterization is not always feasible, and therefore, we need simple noninvasive modalities to replace catheterization.1),2) The initial approach to assess diastolic function was the pulsed-wave Doppler of mitral inflow, based on the early filling (E) and atrial contraction (A) ratio and E-deceleration time. However, there were some limitations, first being its dependency on loading conditions and difficulty in differentiation between the normal and pseudonormal pattern. To overcome these limitations, mitral annular tissue Doppler imaging (TDI), with primary measurements of systolic (s'), early diastolic (e') and late diastolic velocity (a') has been widely used. TDI-derived velocities also have some limitations. The e' velocity can change with increase in age and it may not be useful in conditions of heavy mitral annular calcification, septal or lateral wall infarction, constrictive pericarditis, and severe mitral regurgitation. Despite these limitations, TDI is a sensitive and load-independent measure of LV relaxation, and has been a part of the most widely used and important echocardiographic parameter. A recent study by Baek et al.3) identified that when interpreting diastolic function in elderly subjects, different cut-off values should be considered according to TDI modality, annulus site, and gender. Study results have shown that spectral TDI has a somewhat higher e' than that of color-coded TDI, and the e' value in both these methods of tissue Doppler is lower in women as compared with men.

Surgical and Nonsurgical Complications of a Pig to Baboon Heterotopic Heart Transplantation Model

A modified immunosuppressive regimen, developed at the National Institutes of Health, has been employed in a large animal model of heterotopic cardiac xenotransplantation. Graft survival has been prolonged, but despite this, our recipients have succumbed to various surgical or nonsurgical complications. Herein, we have described different complications and management strategies. The most common complication was hypercoagulability (HC) after transplantation, causing thrombosis of both small and large vasculature, ultimately leading to graft loss. While managing this complication we discovered that there was a delicate balance between HC and consumptive coagulopathy (CC). CC encountered in some recipient baboons was not able to be reversed by stopping anticoagulation and administering multiple blood transfusions. Some complications had iatrogenic components. To monitor the animals, a solid state left ventricular telemetry probe was placed directly into the transplanted heart via the apex. Induction of hypocoagulable states by continuous heparin infusion led to uncontrollable intra-abdominal bleeding in 1 baboon from this apical site. This occurrence necessitated securing the probe more tightly with multiple purse strings and 4-quadrant pledgeted stay sutures. One instance of cardiac rupture originated from a lateral wall infarction site. Earlier studies have shown infections to be uniformly fatal in this transplant model. However, owing to the telemetry placement, infections were identified early by temperature spikes that were treated promptly with antibiotics. We had several cases of wound dehiscence due to recipients disrupting the suture line. These complications were promptly resolved by either re-approximating the wound or finding distractions for the baboon. A few of the most common problems we faced in our earlier experiments were related to the jacket, tether, and infusion pumps. It was difficult to keep the jackets on some baboons and the tether had to be modified several times before we assured long-term success. Infusion catheter replacement resulted in transplant heart venous obstruction and thrombosis from a right common femoral venous line. Homeostatic perturbations such as HC and CC and baboon-induced wound complications comprised most complications. Major bleeding and death due to telemetry implantation and infarct rupture occurred in 2 baboons. Despite the variety of complications, we achieved significant graft prolongation in this model.

Acute pseudoperipheric vertigo and Wallenberg syndrome

We report an atypical Wallenberg syndrome presented with an acute vertigo, preceded by headache, simulating a peripheral vestibular pathology. The first magnetic resonance imaging (MRI) study done in urgencies is negative. Presence of headache, strong lateral ataxia and secondary focally neurological symptoms 48 h after the beginning of the crises, lead to a repetition of the MRI which shows a right lateral bulbar infarct. We focus on the semiological elements that can guide us to a lateral bulbar pathology in patients with pseudoperypheric symptoms (axial lateropulsion, ocular laterodeviation, posterior headache, oculographic test, etc.).

Therapeutic role of rTMS on recovery of dysphagia in patients with lateral medullary syndrome and brainstem infarction

BackgroundThere is some evidence for a therapeutic effect of repetitive transcranial magnetic stimulation (rTMS) on dysphagia in hemispheric stroke.AimTo compare the effect of active or sham rTMS applied to the...

Vértigo agudo pseudoperiférico y síndrome de Wallenberg

We report an atypical Wallenberg syndrome presented with an acute vertigo, preceded by headache, simulating a peripheral vestibular pathology. The first Magnetic Resonance Imaging (MRI) study done in urgencies is negative. Presence of headache, strong lateral ataxia and secondary focally neurological symptoms 48 h after the beginning of the crises, lead to a repetition of the MRI which shows a right lateral bulbar infarct. We focus on the semiological elements that can guide us to a lateral bulbar pathology in patients with pseudoperypheric symptoms (axial latero-pulsion, ocular laterodeviation, posterior headache, oculographic test, etc.).

Superior cerebellar artery infarction in endovascular treatment for tentorial dural arteriovenous fistulas

Background Superior cerebellar artery (SCA) syndrome shows ipsilateral cerebellar ataxia and Horner's syndrome, contralateral superficial sensory disturbance, as well as nystagmus toward the impaired side, vertigo, and nausea. Occasionally, unilateral lesions may produce bilateral hypogeusia and contralateral hypoacusia. Objective To report 2 patients with unilateral lower midbrain ischemic lesions of the inferior colliculus level caused by transarterial embolization for tentorial dural arteriovenous fistulas (TDAVFs). Methods Hospital records for 21 patients with TDAVFs mainly treated by endovascular techniques between 2005 and 2008 were reviewed. Two patients with MRI evidence of unilateral SCA territory infarction were investigated. Results Of 21 patients, 2 treated transarterially with Onyx-18 (a nonahesive liquid embolic agent) developed infarctions in the territory of SCA. One patient had lateral SCA infarction characterized by ipsilateral gait ataxia, contralateral hemihypoesthesia, with additional ipsilateral ocular motor palsy and bilateral gustatory loss. And the other patient had medial SCA infarction characterized by ipsilateral ataxia contralateral hemihypoesthesia with additional contralateral hypoacusia. Conclusion SCA infarction can be caused by transarterial injection of Onyx-18 via SCA or the posterior cerebral artery (PCA) for TDAVFs and additionally presented with gustatory loss and deafness, which is generally not a feature of the SCA syndrome.

Ocular lateropulsion in Wallenberg's syndrome: a prospective clinical study.

In order to evaluate the occurrence and clinical value of ocular lateropulsion in Wallenberg's syndrome, a prospective study was carried out. Lateropulsion of the horizontal and vertical refixation saccades was a rather regular finding, especially in complete Wallenberg's syndrome. Lateral ocular deviation after elimination of fixation was present in nearly all cases. The tonic lateral vector was always directed to the involved side. It is concluded that ocular lateropulsion is an easily elicited sign with a lateralizing value in lateral bulbar infarction. Further systematic search of ocular lateropulsion in other posterior fossa disorders is needed to determine its topographical significance.

Myocardial infarction related to aberrant left circumflex artery

We present a case of lateral wall infarction in the territory of an anomalous circumflex artery without significant stenosis. The unusual location of the infarction suggests a causal relation with the anomalous artery through minor plaque rupture, which may have resulted from mechanical stress.

Acute and Chronic Hemodynamic Effects of Biventricular Pacing in Patients with Coronary Artery Disease and Lateral LV Wall Infarct

Acute and Chronic Hemodynamic Effects of Biventricular Pacing in Patients with Coronary Artery Disease and Lateral LV Wall Infarct

Risk factors, clinical features and outcome of acute myocardial infarction in Sana’a, Yemen

Of all patients, 348 (90.2%) were men with a mean (+/- SD) age 54 +/- 11 years (range, 27-82 years) and 38 (9.8%) were women with a mean age of 59 +/- 11 years (range, 38-80 years). Almost all patients (97.9%) were Yemeni. The prevalence of risk factors was as follows: khat chewing (88%), smoking (81%), total serum cholesterol (29%), diabetes mellitus (25%) and hypertension (18%). When classified according to site, recurrence and severity of AMI, in 57.0% there was an anterior infarction, in 35.2% an inferior infarction,in 7.0% an inferoseptal infarction, in 1.8% a lateral infarction and location was undetermined in 2.5%. Only 34 (8.8%) patients had a previous history of AMI; in 352 (91.2%) patients, it was the first AMI. In 341 (88.3%) it was a Q-wave infarction while a non Q-wave infarction was found in 35 (9.1%) and in 10 (2.6%) it was undetermined. The complications of AMI were heart failure in 94 cases (24.6%), primary ventricular fibrillation or tachycardia in 18 cases (4.7%), and second or third degree atrioventricular block in 17 (4.4%). The ICU mortality rate was 11.4% (44 patients) and the total in-hospital mortality was 14.2% (55 patients). Causes of death during hospitalization were cardiogenic shock (62%), sudden death (18%), resistant arrhythmia (13%), brain embolization (5%), and hypoxic brain damage after CPR (2%).

Risk factors, clinical features and outcome of acute myocardial infarction in Sana′a, Yemen

Of all patients, 348 (90.2%) were men with a mean (+/- SD) age 54 +/- 11 years (range, 27-82 years) and 38 (9.8%) were women with a mean age of 59 +/- 11 years (range, 38-80 years). Almost all patients (97.9%) were Yemeni. The prevalence of risk factors was as follows: khat chewing (88%), smoking (81%), total serum cholesterol (29%), diabetes mellitus (25%) and hypertension (18%). When classified according to site, recurrence and severity of AMI, in 57.0% there was an anterior infarction, in 35.2% an inferior infarction,in 7.0% an inferoseptal infarction, in 1.8% a lateral infarction and location was undetermined in 2.5%. Only 34 (8.8%) patients had a previous history of AMI; in 352 (91.2%) patients, it was the first AMI. In 341 (88.3%) it was a Q-wave infarction while a non Q-wave infarction was found in 35 (9.1%) and in 10 (2.6%) it was undetermined. The complications of AMI were heart failure in 94 cases (24.6%), primary ventricular fibrillation or tachycardia in 18 cases (4.7%), and second or third degree atrioventricular block in 17 (4.4%). The ICU mortality rate was 11.4% (44 patients) and the total in-hospital mortality was 14.2% (55 patients). Causes of death during hospitalization were cardiogenic shock (62%), sudden death (18%), resistant arrhythmia (13%), brain embolization (5%), and hypoxic brain damage after CPR (2%).

Pathological Hyperfamiliarity for Others From a Left Anterior Cingulate Lesion

Back to table of contents Previous article Next article LETTERFull AccessPathological Hyperfamiliarity for Others From a Left Anterior Cingulate LesionFrancisco Nente M.D.,Roger Carrillo-Mezo M.D.,Mario F. Mendez M.D.,Jesus Ramirez-Bermudez M.D., M.Sc.,Francisco Nente M.D.Search for more papers by this author,Roger Carrillo-Mezo M.D.Search for more papers by this author,Mario F. Mendez M.D.Search for more papers by this author,Jesus Ramirez-Bermudez M.D., M.Sc.Search for more papers by this author,Published Online:1 Jul 2007AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail SIR: Person misidentification syndromes usually involve the misperception of familiar persons or a loss of familiarity for normally perceived ones. We report a unique patient who developed the opposite, a sense of hyperfamiliarity for unfamiliar persons after a hemorrhage in the left anterior cingulate cortex (ACC). Case ReportA 34-year-old man developed an acute onset of a severe headache, followed by transient loss of alertness. He spontaneously recovered but 2 days later was hospitalized because of new-onset generalized seizures. The patient had a negative medical history and was on no medications at the time of admission.On initial examination, he was in a postictal delirium. He had otherwise normal examinations of his cranial nerves, motor systems, and reflexes. He was loaded with phenytoin without further seizures. A computed tomography (CT) scan revealed a hyperdense region located in the left anterior cingulate cortex consistent with a hemorrhage. Angiography and magnetic resonance imaging (MRI) revealed a cavernous angioma. On electroencephalography, there were theta waves in the left frontocentral region.One day after admission, mental status examination revealed an akinetic mute state. He was totally indifferent to external stimuli. Over the following days, the patient had gradually increasing verbal output and behavioral initiation. On day 7 after admission, neurobehavioral testing revealed normal orientation, attention, language, constructional abilities, calculation, reasoning, and judgment with impairment in verbal learning.Surprisingly, the patient repeatedly expressed strong sensations of having previously known many of the hospital personnel. Sometimes he would ask if he knew them from school or his hometown, a rural village. The patient recognized that his feelings of familiarity were incorrect and strange but he continued to report the presence of these feelings. His sense of hyperfamiliarity for strangers gradually disappeared over a 2-week period, and he was discharged fully recovered.Comment The present case provides further evidence for the “assoziierende Erinnerungs- falschungen” phenomenon, or the sensation that unknown people are already known, originally described by Emil Kraepelin. 1 This person hyperfamiliarity syndrome is distinct from Fregoli’s phenomenon, in which strangers are identified as familiar persons. 2 Fregoli patients change the personal identities of surrounding persons, but this patient only felt that they were familiar and did not change their identities. This patient had a focal lesion in the left ACC, or Brodmann’s Area 24. This corresponds to the “affect” region of the ACG, which regulates emotional awareness, as well as motivation and intention. Consistent with this localization, this patient had an initial akinetic muteness. His subsequent hyperfamiliarity syndrome implies that an alteration in emotional awareness for people is mediated by the ACC. Prior investigations have suggested a right hemisphere person recognition network that links seen faces with representations of affective and personal relevance. 3 – 5 The right superior temporal gyrus, amygdala, and orbitofrontal cortex respond to facial emotions and contribute to a sense of familiarity from faces. 1 – 4 Hyperfamiliarity for unknown faces could arise from a hemispheric imbalance, with relative hypoactivation of left hemisphere processes but hyperactivation and spurious responsiveness of the right hemisphere person recognition network. 5Neuropsychiatry Unit, National Institute of Neurology and Neurosurgery of MexicoNeuroimaging Department, National Institute of Neurology and Neurosurgery of MexicoDepartment of Neurology, University of California, Los Angeles, CaliforniaNeuropsychiatry Unit, National Institute of Neurology and Neurosurgery of MexicoReferences1 . Murai T, Kubota Y, Sengoku A: Unknown people believed to be known: the “assoziierende Erinnerungs- falschungen” by Kraepelin. Psychopathology 2000; 33:52–54Google Scholar2 . Dugall HS: Interictal psychosis presenting with Fregoli syndrome. J Neuropsychiatry Clin Neurosci 2004; 16:543–544Google Scholar3 . Mandal MK, Asthana HS, Maitra S: Right hemisphere damage impairs the ability to process emotional expressions of unusual faces. Behav Modif 1998; 22:167–176Google Scholar4 . Stone A, Valentine T: Perspectives on prosopagnosia and models of face recognition. Cortex 2003; 39:31–40Google Scholar5 . Vuilleumier P, Mohr C, Valenza N, et al: Hyperfamiliarity for unknown faces after left lateral temporo-occipital venous infarction: a double dissociation with prosopagnosia. Brain 2003; 126:889–907Google Scholar FiguresReferencesCited byDetailsCited ByA case of encephalitis with hyperfamiliarity for facesRinsho Shinkeigaku, Vol. 55, No. 7Epilepsy & Behavior, Vol. 25, No. 2Cotard Syndrome in Neurological and Psychiatric PatientsJesus Ramirez-Bermudez, M.D., M.Sc.Luis C. Aguilar-Venegas, M.D.Daniel Crail-Melendez, M.D., M.Sc.Mariana Espinola-Nadurille, M.D.Francisco Nente, M.D.Mario F. Mendez, M.D., Ph.D.1 October 2010 | The Journal of Neuropsychiatry and Clinical Neurosciences, Vol. 22, No. 4 Volume 19Issue 3 Summer, 2007Pages 345-346 Metrics PDF download History Published online 1 July 2007 Published in print 1 July 2007

Ultrasonic and pathological evidence of a neo-intimal plaque rupture in patients with bare metal stents

Case 1 A 58-year-old man was admitted to our coronary care with troponin negative unstable angina. His risk factors included, being an exsmoker for a year, treated hypertension and dyslipidaemia. Medication on admission was aspirin and a statin. ECG showed Twave inversion laterally. Nine years previously he had a bare metal stent implanted in his circumflex artery following a lateral infarction the preceding year. Angiography done during his acute presentation revealed an in-stent restenosis in the previously treated circumflex artery and a diffusely diseased marginal branch. The left anterior decending coronary (LAD) was normal and the right coronary artery (RCA) had a non-flow limiting lesion in the mid-vessel with a fractional flow reserve (FFR) of 0.79. Intravascular ultrasound (IVUS) of the circumflex artery was performed using a 20 MHz Eagle eye IVUS catheter (Volcano Therapeutics, Rancho Cordova, CA, USA). The length of the stented segment was 30mm and had a minimal luminal area (MLA) 4.6 mm2. Neo-intimal formation was visible throughout the stent (Figure 1). This gave a neointimal hyperplasia (NIH) volume of 80.3 mm3. The NIH on virtual histology had a tissue composition of necrotic core (NC) 13.6%, (0.08 mm2, 2.4 mm3), calcified tissue 16.8%, (0.10 mm2, 3.0 mm3), fibrofatty 5.8%, (0.03 mm2, 1.04 mm3), fibrotic tissue 63.9%, (0.38 mm2, 11.5 mm3). Distal to the MLA at distance of 18 mm IVUS revealed an eccentric soft neo-intimal ruptured plaque1,2 (Figure 1C) within the stent. The necrotic core was 22% with remnant plaque burden of 54% at the plaque rupture site (Figure 1 C’). Just distal to ruptured plaque the vessel wall was intact and the plaque burden was higher 65% with no necrotic core in contact with the lumen (Figure 1D”). This ruptured lesion was subsequently managed with a drug eluting stent (DES) that also covered the MLA. The histological findings of a similar plaque rupture are illustrated in Case 2.

Noncompaction of the ventricular myocardium mimicking ischemic cardiomyopathy

A 68-year-old woman was admitted to our hospital because of left ventricular failure. Myocardial perfusion single-photon emission computed tomography demonstrated a non-reversible perfusion defect in the anterolateral left ventricular segments and reduced ejection fraction, findings consisted with ischemic cardiomyopathy accompanied by lateral wall infarction. Coronary angiogram was normal, but the left ventriculogram showed prominent trabeculations in the apical and anterolateral segments. The left ventricular ejection fraction was 28%. Cine magnetic resonance imaging demonstrated prominent trabeculations and deep intertrabecular recesses, findings consistent with noncompaction of the ventricular myocardium. Myocardial hypoperfusion or necrosis in the noncompacted myocardium may be the cause of myocardial damage and possibly the basis of left ventricular failure.

Non-Invasive Visualization of the Cardiac Venous System in Coronary Artery Disease Patients Using 64-Slice Computed Tomography

This study was designed to evaluate the value of 64-slice computed tomography (CT) to visualize the cardiac veins and evaluate the relation between variations in venous anatomy and history of infarction. Cardiac resynchronization therapy (CRT) is an attractive treatment for selected heart failure patients. Knowledge of venous anatomy may help in identifying candidates for successful left ventricular lead implantation. The 64-slice CT of 100 individuals (age 61 +/- 11 years, 68% men) was studied. Subjects were divided into 3 groups: 28 control patients, 38 patients with significant coronary artery disease (CAD), and 34 patients with a history of infarction. Presence of the following coronary sinus (CS) tributaries was evaluated: posterior interventricular vein (PIV), posterior vein of the left ventricle, and left marginal vein (LMV). Vessel diameters were also measured. Coronary sinus and PIV were identified in all individuals. Posterior vein of the left ventricle was observed in 96% of control patients, 84% of CAD patients, and 82% of infarction patients. In patients with a history of infarction, a LMV was significantly less observed as compared with control patients and CAD patients (27% vs. 71% and 61%, respectively, p < 0.001). None of the patients with lateral infarction and only 22% of patients with anterior infarction had a LMV. Regarding quantitative data, no significant differences were observed between the groups. Non-invasive evaluation of cardiac veins with 64-slice CT is feasible. There is considerable variation in venous anatomy. Patients with a history of infarction were less likely to have a LMV, which may hamper optimal left ventricular lead positioning in CRT implantation.