Spontaneous Epidural Hematoma of the Cervical Spine Following Thrombolysis in a Patient with STEMI-Two Medical Specialties Facing a Rare Dilemma.

Spontaneous spinal epidural hematoma (SSEH) is a rare, albeit well-documented complication following thrombolysis treatment in ST elevation myocardial infarction (STEMI). A SSEH usually manifests with cervical pain and neurologic deficits and may require surgical intervention. In this case report, we present the first reported SSEH to occur following thrombolysis with reteplase. In this case, the SSEH manifested with cervical pain shortly after the patient emerged from his rescue percutaneous coronary intervention (PCI). Although magnetic resonance imaging reported spinal cord compression, the lack of neurologic symptoms prompted the treating clinicians to delay surgery. A dangerous dilemma emerged, as the usual antithrombotic regimen that was necessary to avoid stent thrombosis post-PCI, was also likely to exacerbate the bleeding. As a compromise, the patient only received aspirin as a single antiplatelet therapy. Ultimately, the patient responded well to conservative treatment, with the hematoma stabilizing a week later, without residual neurologic deficits. In conclusion, the conservative treatment of SSEH appears to be an acceptable option for carefully selected patients, but the risks of permanent neurologic deficits and stent thrombosis have to be weighted for each patient.

Spontaneous Coronary Artery Dissection (SCAD): Case Series and Mini Review.

Spontaneous coronary artery dissection (SCAD) has gained recognition in recent years as a non-atherosclerotic cause of acute coronary syndrome (ACS), especially in young and middle-aged women without any of the classic risk factors for cardiovascular disease. The booming use of coronary angiography in patients presenting with ACS combined with new, revolutionary methods of intravascular imaging, have led to increased rates of SCAD diagnosis. We aim to present a brief, up-to-date review of the existing literature, along with our experience as reflected in the recent management of nine SCAD cases in three tertiary care hospitals.

Left atrial deformation as a potent predictor for paroxysmal atrial fibrillation in patients with end-stage renal disease.

It is widely known that various factors contribute to left atrial (LA) mechanical dysfunction in patients with end stage renal disease (ESRD). However, the connection between atrial dysfunction and arrhythmic events such as paroxysmal atrial fibrillation (PAF), in this group of patients, remains unclear. The purpose of our study was to evaluate prospectively the association between LA deformation indices and PAF in ESRD patients. 79 patients (41 men, mean age 57 ± 17) with ESRD and preserved left ventricular systolic function comprised the study population. All patients underwent a baseline comprehensive echocardiography study and were followed for a mean period of 16 ± 5 months. PAF episodes, first and the following events, were reported. LA longitudinal strain reflecting LA reservoir function and LA longitudinal strain rate reflecting LA pump function were specifically evaluated as LA deformation indices of interest, using 2D speckle tracking echocardiography. At the end of follow up period nine patients died. 15 of the rest 70 reported one or more episodes of PAF. LA indexed volumes were significantly higher in patients with PAF (32 ± 26 vs. 21.5 ± 9 ml/m2, p = 0.002), mean LA strain was significantly reduced (17 ± 7 vs. 27 ± 9%, p < 0.001) as well as mean LA stain rate (- 1.19 ± 0.5 vs. - 1.95 ± 0.5 1/s, p < 0.001). Multivariate analysis showed that LA strain rate when adjusted with age together with PAF history remained the single most significant echocardiographic parameter for PAF prediction. Impaired LA strain and LA strain rate are associated with PAF in ESRD patients. LA strain rate might be a better independent predictor of PAF, compared to standard echocardiographic indices. Further prospective studies are needed to validate its relevance in routine clinical practice.

Beneficial effect of ischemic preconditioning on post-infarction left ventricular remodeling and global left ventricular function.

BACKGROUND: Preinfarction angina (PA) is a clinical analogue of ischemic preconditioning that improves postinfarct prognosis. Data concerning the association of PA with post infarction left ventricular (LV) remodeling and LV diastolic function are limited. We aimed to evaluate this association in patients with acute myocardial infarction (AMI) in the modern clinical era of widespread use of revascularization and antiremodeling medical treatment. METHODS: We studied 53 patients with anterior AMI who underwent complete reperfusion and received up to date antiremodeling medical treatment. LV remodeling, systolic and diastolic function were assessed using 2D echocardiography at baseline and 6 at months follow-up. Patients were divided into two groups regarding the presence or absence of PA. RESULTS: LV remodeling at follow-up was less frequent in the PA group (25 vs. 55 %, P<.05). Patients with PA had lower end-systolic volume index at baseline and follow up (24.1±6 vs. 30.1±14 ml/m(2), P<.001 and 25.3±8 vs. 35.6±2 ml/m(2), P=.001 respectively). Additionally at 6 months, they had better LV ejection fraction (52.1±9 vs. 42.9±10 %, P=.002) and exhibited improved diastolic filling as reflected by mitral E/e' (14.6±5 vs. 18.8±8, P=.05). CONCLUSIONS: Ischemic preconditioning in the form of PA promotes better LV systolic and diastolic function in the mid-term and is associated with less postinfarct LV remodeling in this specific study population. The results of the study underline the possible need for further risk stratification of AMI patients regarding the absence of PA.

Trimetazidine administration minimizes myocardial damage and improves left ventricular function after percutaneous coronary intervention.

BACKGROUND AND OBJECTIVE: The aim of this study was to evaluate whether the administration of trimetazidine, a piperazine derivative, to patients before and after percutaneous coronary intervention (PCI) minimizes the PCI-induced myocardial damage and improves left ventricular function 1 and 3 months after the procedure. METHODS: Fifty-two patients hospitalized for acute coronary syndromes (ACS) were included in this study. Patients were randomized into two groups: group A (trimetazidine group; n = 27) and group B (placebo group; n = 25). All patients received conventional antianginal therapy. In addition, group A patients received oral trimetazidine 20 mg every 8 hours, starting 15 days before PCI and continuing for 3 months after the procedure. For each patient, serum troponin I and creatinine kinase (CK)-MB levels were measured before PCI, then at 6, 24, and 48 hours after the procedure; a 2D cardiac echocardiogram was performed before PCI and at 1 and 3 months after the procedure. RESULTS: Twenty-four hours after PCI, troponin I levels were >1 ng/mL in 7 of 27 patients (26%) of group A and 11 of 25 patients (44%) in group B. Fourty-eight hours after revascularization troponin levels remained elevated in 15% of patients in group A and in 32% of patients in group B. Twenty-two percent of patients in group A had CK-MB levels >5 ng/mL, 24 hours after PCI, compared with 40% of patients in group B; four patients of group A had high CK-MB levels prior to PCI procedure. Echocardiographic measurements before revascularization revealed that 11 of 27 patients (40%) in group A had an ejection fraction <50% versus 8 of 24 patients (33%) in group B . The number of patients with an ejection fraction <50% was significantly reduced in group A compared with group B at 1 and 3 months after PCI, i.e. 11% versus 16% (p = 0.046) at 1 month and 4% versus 16% (p = 0.017) at 3 months.A significant improvement in regional wall motion was noted after treatment with trimetazidine compared with placebo. One month after PCI, inferior left ventricular (LV) wall hypokinesia had improved in 4 of 6 trimetazidine recipients and in 4 of 14 placebo recipients (p = 0.014, group A vs group B). After 3 months inferior wall hypokinesia improved in four patients in group A versus six patients in group (p = 0.05). Similarly, anterior LV wall motion improved in 3 of 11 patients in group A and in 1 of 6 patients in group B at 1 month. After 3 months anterior wall hypokinesia had improved in eight patients in group A and in two patients in group B (p = 0.04, group A vs group B). CONCLUSION: The metabolic agent trimetazidine appears to minimize myocardial reperfusion injury during PCI and improves global and regional wall motion at 1 and 3 months after PCI. This study was limited by small patient numbers and further studies are necessary to evaluate exact mechanisms of action and clinical implications of using trimetazidine in conjunction with PCI.

Severe case of Mediterranean spotted fever in Greece with predominantly neurological features.

Rickettsia conorii is endemic in Greece, though only a few cases of infection have been published to date. The case of a 58-year-old man from northern Greece with a severe form of Mediterranean spotted fever and rapid neurological deterioration is presented here. The patient received antibiotic treatment with doxycycline, showing immediate clinical and laboratory improvement. Diagnosis was confirmed later, during the second week after disease onset, by detection of elevated titres of IgM and IgG antibodies against R. conorii using an indirect immunofluorescence assay.

Phospholamban gene mutations are not associated with hypertrophic cardiomyopathy in a Northern Greek population.

Hypertrophic cardiomyopathy (HCM) is a genetically transmitted cardiac disease characterized by unexplained myocardial hypertrophy and diverse clinical spectrum. Currently, more than 250 HCM-related mutations in 10 genes encoding contractile sarcomeric proteins have been identified. Phospholamban (PLN) is a modest modulator of intracellular Ca2+ homeostasis and may be a candidate gene responsible for cardiomyopathy. In this study 53 consecutive patients with HCM, coming from Northern Greece, were screened for mutations of PLN gene. The patients were evaluated by clinical history, physical examination, electrocardiogram and echocardiography. All PCR products were analyzed for mutation by both restriction analysis and sequencing. The systematic mutation screening did not reveal any mutation in exons 1 and 2 or in the promoter region of phospholamban gene. Additionally, no polymorphisms were detected in all patients. Therefore, PLN gene mutations were not found to be associated with HCM in a Northern Greece population.