Konstantinos Vlasis

The Pterygopalatine Ganglion and its Role in Various Pain Syndromes: From Anatomy to Clinical Practice

Abstract  The postsynaptic fibers of the pterygopalatine or sphenopalatine ganglion (PPG or SPG) supply the lacrimal and nasal glands. The PPG appears to play an important role in various pain syndromes including headaches, trigeminal and sphenopalatine neuralgia, atypical facial pain, muscle pain, vasomotor rhinitis, eye disorders, and herpes infection. Clinical trials have shown that these pain disorders can be managed effectively with sphenopalatine ganglion blockade (SPGB). In addition, regional anesthesia of the distribution area of the SPG sensory fibers for nasal and dental surgery can be provided by SPGB via a transnasal, transoral, or lateral infratemporal approach. To arouse the interest of the modern‐day clinicians in the use of the SPGB, the advantages, disadvantages, and modifications of the available methods for blockade are discussed.▪

Novel Biomarkers Assessing the Calcium Deposition in Coronary Artery Disease

Coronary atherosclerosis is the pathophysiologic background of coronary artery disease. Vascular calcification is an actively regulated form of calcified tissue metabolism and a common feature of coronary atherosclerotic plaques. Interestingly, systematic research has revealed that vascular mineralization, is also a strong and independent predictor of cardiovascular morbidity and mortality. Recently, several biomarkers, including osteopontin, fetuin-A, matrix-carboxyglutamic acid protein, pyrophosphates, bone morphogenetic proteins, leptin, osteoprotegerin have emerged as surrogate markers of coronary calcification. Furthermore, biomarkers of vascular calcification can be used as prognostic markers of coronary artery disease and can predict future cardiovascular events and mortality. Nevertheless, there is little knowledge on the usefulness of these biomarkers in evaluating the results of treatments targeting coronary artery disease. Within this context, the present review sets out to discuss the role of new biomarkers assessing calcium deposition in coronary arteries and their role in the prognosis, progression, and treatment of cardiovascular disease.

The Role of Endothelial Dysfunction in Aortic Aneurysms

Abdominal aortic aneurysm is a vascular disease which, despite the fact that it shares common risk factors with atherosclerosis, develops in parallel but as a partly independent process, through different pathogenic mechanisms. The pathogenic mechanisms involve metalloproteinase and collagenase activation, median and adventitial degradation, elastin lysis, vascular smooth cells transformation and apoptosis, collagen production and lysis imbalance combined with excessive inflammatory infiltration. Endothelial cells respond to a number of stimulating factors, including smoking, hypertension and AT1 receptor stimulation and non-uniform distribution of wall stress. Their ability to produce NO is crucial in order to adapt. Endothelial cells contribute to AAA development due to increased oxidative stress which is partly mediated by impaired NO bioavailability due to endothelial dysfunction and NADPH oxidase overexpression. In addition, they express several molecules among which adherence molecules, selectins, endothelin-1, regulating inflammatory infiltration and oxidative stress. Inflammatory cells consist of monocytes, polymorphonuclear neutrophils and lymphocytes and they are involved in the degrading process in the aortic wall by secreting proteolytic enzymes or by releasing interleukins which mediate the inflammation response. Endothelial dysfunction and arterial stiffness reflect on indices like FMD, carotid-femoral PWV and augmentation index, sometimes with controversial results. At present, surgical treatment is the only option provided in patients with large AAA, in particular. Focusing on the emerging role of endothelial cells in AAA pathology may contribute in creating new therapeutic options in a disease which has not yet a well-accepted, implemented pharmaceutical treatment.

Inflammation in lone atrial fibrillation: New insights by coronary sinus thermography

BACKGROUND In the clinical setting there are conflicting results regarding the role of inflammatory activation in atrial fibrillation (AF). Coronary sinus (CS) thermography assesses myocardial heat production and is correlated with inflammatory states. We investigated in patients with AF whether 1) there is increased CS blood temperature and 2) the correlation of heat production with systemic inflammation. METHODS We included patients with AF and subjects with sinus rhythm. C-reactive protein (CRP) levels were measured in all patients. CS and right atrium (RA) blood temperature measurements were performed by a dedicated 7F thermography catheter. DeltaT was calculated by subtracting RA from CS blood temperature. RESULTS We included 47 patients with AF and 23 subjects with sinus rhythm. We stratified patients with AF into two groups: normotensive (AFN) and hypertensive (AFH). DeltaT was lower in the RA compared with the CS in AFH (37.27+/-0.52 degrees C vs 37.47+/-0.54 degrees C, p<0.01), in AFN (37.13+/-0.53 degrees C vs 37.34+/-0.54 degrees C, p<0.01), and in controls (37.41+/-0.69 degrees C vs 37.55+/-0.68 degrees C, p<0.01). DeltaTau was greater in AFH, and AFN compared to controls (0.20+/-0.07 degrees C, 0.20+/-0.08 degrees C, vs 0.14+/-0.06 degrees C, p<0.01). DeltaT was similar between AFH and AFN (p=0.95). CRP was higher in AFH and AFN compared to controls (1.72+/-0.85 mg/Dl, 1.69+/-0.94 mg/dL, 0.98+/-0.71 mg/dL, p<0.01). CRP was similar between AFH and AFN (p=0.87). A correlation between CRP with DeltaT was observed in AFH and AFN (R=0.58, p<0.01, R=0.44, p=0.02). CONCLUSIONS Patients with AF have increased myocardial heat production, which is correlated to the systemic inflammation. CS blood temperature measurement may provide significant information for the pathogenesis of AF.

Vascular function and ocular involvement in sarcoidosis.

Ocular involvement occurs in sarcoidosis (Sar) patients mainly in the form of uveitis. This study was designed to determine if uveitis in Sar patients is associated with vascular impairment. We enrolled 82 Sar patients and 77, age and sex matched, control subjects (Cl). Sar patients were divided into those with ocular sarcoidosis (OS) and those without ocular sarcoidosis (WOS). Endothelial function was evaluated by flow-mediated dilation (FMD). Pulse wave velocity (PWV) was measured as an index of aortic stiffness and augmentation index (AIx) as a measure of arterial wave reflections. Although there was no significant difference in sex, age and mean arterial pressure, patients with OS compared to WOS patients and Cl subjects had impaired FMD (p<0.001), increased AIx (p=0.02) and increased PWV (p=0.001). Interestingly, impaired FMD in Sar patients was independently, from possible covariates (age, sex, smoking habits, arterial hypertension, dyslipidemia), associated with increased odds of ocular involvement (odds ratio=1.69, p=0.001). More precisely ROC curve analysis revealed that FMD had a significant diagnostic ability for the detection of OS (AUC=0.77, p<0.001) with a sensitivity of 79% and a specificity of 68% for an FMD value below 6.00%. To conclude in the present study we have shown that ocular involvement in Sar patients is associated with impaired endothelial function and increased arterial stiffness. These results strengthen the vascular theory which considers uveitis a consequence of vascular dysfunction in Sar patients and reveals a possible clinical importance of the use of endothelial function tests.

Clopidogrel response variability is associated with endothelial dysfunction in coronary artery disease patients receiving dual antiplatelet therapy.

OBJECTIVES Dual antiplatelet therapy with aspirin and a platelet P2Y12 ADP receptor antagonist is the cornerstone of treatment following percutaneous coronary intervention (PCI). Several clinical and genetic factors can cause suboptimal clopidogrel response. We examined the impact of endothelial dysfunction on clopidogrel response variability in subjects with stable coronary artery disease (CAD) after PCI. METHODS We consecutively enrolled 198 patients with stable CAD one month after successful PCI. All patients were receiving dual antiplatelet therapy (clopidogrel 75 mg and aspirin 100 mg/day). Platelet reactivity was measured by VerifyNow P2Y12 assay (Accumetrics, San Diego, CA). VerifyNow reports its results in P2Y12 reaction units (PRU) and the diagnostic cut-off value is 230. Endothelial function was evaluated by flow mediated dilation (FMD). RESULTS Patients with high on treatment platelet reactivity (32% of the study population), compared to subjects with low on treatment platelet reactivity, presented decreased FMD values (4.35 ± 2.22% vs. 5.74 ± 3.29%, p = 0.01). Moreover, an inverse association between endothelial function measurement and platelet reactivity (r = -0.24, p = 0.001) was found. Importantly, multivariate analysis after adjustment for age, gender and confounders revealed by the univariate analysis (left ventricle ejection fraction, body mass index, diabetes, dyslipidemia, coronary lesion number) showed that for every decrease in FMD by 1% there is an anticipated increased in the odds of patients to have HPR by 1.66 (95% CI 1.03-2.57, p = 0.037). CONCLUSIONS Endothelial dysfunction is associated with clopidogrel response variability in patients after PCI receiving dual antiplatelet therapy. These findings shed some light on the mechanisms affecting individual platelet response to antiplatelet therapy and may explain the non-straight forward association between clopidogrel dose, platelet inhibition and cardiovascular outcome.

Circulating Biomarkers Determining Inflammation in Atherosclerosis Progression.

Atherosclerosis is the main underlying pathology of cardiovascular disease and is precipitated by various hereditary and non-hereditary risk factors. Inflammation is considered an important step in the progression of atherosclerosis and involves numerous cells, mediators and cellular procedures. Therefore, a biomarker able to determine the vascular inflammatory status is imperative as the combination of inflammatory biomarkers with the classic risk factors might provide further information about atherosclerosis progression and cardiovascular risk. The identification of novel inflammatory molecules and the improvement in analytical methods allows the potential implementation of these tests in every day clinical practice. In the current article, we focus on the role of established and novel biomarkers in atherosclerosis progression and in the determination of cardiovascular risk. We also present recent data concerning the risk stratification of patients according to their inflammatory status and the possible anti-inflammatory treatment strategies.

Bilateral Abnormal Origin of the Anterior Branches of the External Carotid Artery

BACKGROUND Description of a rare variation is provided alongside with a review of the literature with special references to anatomic, embryologic, and clinical issues it may create. METHODS This was a cadaveric dissection conducted during a pregraduate anatomy course that is accompanied by short review of the literature and critical appraisal. RESULTS During dissection of the neck region of a male cadaver, the superior thyroid artery occurred from the common carotid artery bilaterally and the lingual artery occurred from the carotid bifurcation on the left side. CONCLUSIONS Superior thyroid artery originating from common carotid artery or carotid bifurcation is a common variation, but the lingual artery originating from the common carotid artery or carotid bifurcation is very rare (<1%). Its existence can have a significant impact on treatment success and potentially lead to errors during interventions at the neck region. A high level of suspicion is required.