The impact of the extent and severity of coronary artery disease on fractional flow reserve measurements.

OBJECTIVE: Coronary angiography has a limitation to determine the severity of intermediate stenosis (30-70%)1,2. Fractional flow reserve (FFR) is a method for the assessment of the intermediate stenosis severity3. The effect of coronary artery disease (CAD) severity on the FFR results is not clear. In this study, we aimed to expose the effect of CAD severity calculated with Syntax and Gensini scores on FFR results. PATIENTS AND METHODS: We scanned patients data (n=378) who had undergone fractional flow reserve measurements in our center. Patients with acute coronary syndrome in the last month, moderate or severe valvular diseases, acute heart failure, serious bradycardia, atrial fibrillation/flutter, severe left ventricular hypertrophy or patient with deficient data were excluded. 351 patients were included in the study. Syntax and Gensini scores were calculated and compared with FFR results. Hemodynamically significant result for FFR, ratio <0.80 was accepted. RESULTS: The negative correlation between high Gensini, high Syntax scores and FFR results was statistically significant. Especially patients with Syntax scores >22 had notable more crucial lesions in FFR measurements (p<0.001). Cardiovascular disease risk factors such as age, gender, hypertension, diabetes mellitus and dyslipidemia did not correlate with the FFR results. Patients with intermediate stenosis (30-70%) and high Gensini and high Syntax scores were found to have more hemodynamically significant on FFR measurements (FFR <0.80). CONCLUSIONS: Intermediate lesions with high Syntax score should be evaluated by hemodynamic procedures and treated more carefully with optimal medical treatment or revascularization. Revascularization method of CAD with high Syntax score should be decided with hemodynamic procedures as FFR measurements.

The MOGE(S) classification : A TNM-like classification for cardiomyopathies.

Cardiomyopathy is a disease of the heart muscle resulting from genetic defects, cardiac myocyte injury, or infiltration of the myocardium. Cardiomyopathies are traditionally defined as dilated, restrictive, and hypertrophic cardiomyopathy. Today, the genetic basis of most diseases has been clearly defined and has influenced the approach to familial diseases such as cardiomyopathies. Traditional definitions of cardiomyopathies, such as those by the American Heart Association and the European Society of Cardiology, do not consider the genetic basis of cardiomyopathies. In 2013, the World Heart Federation added the genetic basis of cardiomyopathies and proposed a descriptive genotype-phenotype nosology system termed "MOGE(S)." The MOGE(S) system resembles the TNM classification system for malignancy, and therefore it can be useful for the diagnosis, management, and treatment of cardiomyopathies in a similar manner to cancer management.

Pseudoaneurysm of the mitral-aortic intervalvular fibrosa. A new comprehensive review.

Pseudoaneurysm of the mitral-aortic intervalvular fibrosa (P-MAIVF) is an infrequent but potentially life-threatening condition. Both transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE) can detect P-MAIVF with sensitivity rates of 43 and 90 %, respectively. The typical finding of echocardiography is a pulsatile echo-free sac that expands in systole and collapses in diastole. Our review comprises 166 patients with P-MAIVF, including eight cases in our hospital and 158 cases from the literature. P-MAIVF is often associated with infection or surgical trauma. While it is likely to maintain an asymptomatic course, symptoms of shortness of breath, heart failure, valvular disease, chest pain, endocarditis, and cerebrovascular events are common clinical presentations. The recommended treatment is surgery. However, conservative therapy is an alternative approach for high-risk patients or when surgical treatment is refused. With the increasing incidence of cardiac surgery and infective endocarditis, a likely increment in the new diagnosis of pseudoaneurysm is expected.

Right coronary artery emerging as a septal branch from the left anterior descending artery: a single coronary ostium anomaly.

Coronary artery anomalies are detected on approximately 1.3% of coronary angiograms. Single coronary artery anomaly (SCA) is defined as the coronary artery arising from a single coronary ostium, nourishing the entire heart. SCA anomalies are usually benign; however, serious complications such as sudden cardiac death and myocardial infarction resulting from these anomalies are also reported in the literature. We report the anomalous origin of the right coronary artery (RCA) as a continuum of the septal branch from the left anterior descending (LAD) artery, which is a very rare variation of a single coronary artery.

Q-VD-OPh, a pancaspase inhibitor, reduces trauma-induced apoptosis and improves the recovery of hind-limb function in rats after spinal cord injury.

BACKGROUND: Various caspases have been implicated in the development of secondary damage after spinal cord injury (SCI). Anticaspase therapy that targets only one caspase has been investigated in a variety of in vitro and in vivo studies. This study examined the neuroprotective effects of Q-VD-OPh, a pan-caspase inhibitor, in a rat model of SCI. METHODS: Thirty Wistar albino rats were divided into 3 groups of 10 each: the sham-operated controls (group 1), the trauma-created controls (group 2), and the QVD- OPh-treated rats (group 3). An SCI (a trauma of 40 g-cm) was produced at the thoracic level (T8-T10) by the weight-drop technique. The response to injury and the neuroprotective effects of Q-VD-OPh were investigated by histopathologic examination and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) 24 hours and 5 days after trauma. The inclined plane technique of Rivlin and Tator and a modified version of Tarlov's grading scale were used to assess the functional status of the rats 24 hours, 3 days, and 5 days after injury. RESULTS: Twenty-four hours after trauma, light microscopic examination of a specimen taken from group 2 rats revealed hemorrhage, necrosis, vascular thrombi, and edema. Group 3 tissue samples showed similar features at that time. Twenty-four hours after trauma, the mean apoptotic cell number was 4.47 +/- 0.35 cells in group 2 and 1.58 +/- 0.33 in group 3. Five days after injury, the mean apoptotic cell count was 4.35 +/- 0.47 in group 2 and 1.25 +/- 0.34 in group 3. Thus the number of TUNEL-positive cells in an injured spinal cord was greatly reduced by treatment with Q-VDOPh. The neurologic function scores (both the inclined plane performance and motor grading scores) were significantly better in the Q-VD-OPh-treated group than in the trauma-created control group. CONCLUSION: The marked antiapoptotic properties of Q-VD-OPh due to the inhibition of all caspases render it a promising novel agent. A therapeutic strategy using Q-VD-OPh may eventually lead to the effective treatment of SCI in humans.

Q-VD-OPh, a pancaspase inhibitor, reduces trauma-induced apoptosis and improvesthe recovery of hind-limb function in rats after spinal cord injury

Background. Various caspases have been implicatedin the development of secondary damage after spinalcord injury (SCI). Anticaspase therapy that targets onlyone caspase has been investigated in a variety of in vitroand in vivo studies. This study examined the neuroprotectiveeffects of Q-VD-OPh, a pan-caspase inhibitor, ina rat model of SCI.Methods. Thirty Wistar albino rats were divided into3 groups of 10 each: the sham-operated controls (group1), the trauma-created controls (group 2), and the QVD-OPh–treated rats (group 3). An SCI (a trauma of40 g-cm) was produced at the thoracic level (T8-T10) bythe weight-drop technique. The response to injury andthe neuroprotective effects of Q-VD-OPh were investigatedby histopathologic examination and terminaldeoxynucleotidyl transferase dUTP nick-end labeling(TUNEL) 24 hours and 5 days after trauma. The inclinedplane technique of Rivlin and Tator and a modifiedversion of Tarlov’s grading scale were used to assess thefunctional status of the rats 24 hours, 3 days, and 5 daysafter injury.Results. Twenty-four hours after trauma, lightmicroscopic examination of a specimen taken fromgroup 2 rats revealed hemorrhage, necrosis, vascularthrombi, and edema. Group 3 tissue samples showedsimilar features at that time. Twenty-four hours aftertrauma, the mean apoptotic cell number was 4.47 ± 0.35cells in group 2 and 1.58 ± 0.33 in group 3. Five daysafter injury, the mean apoptotic cell count was 4.35 ±0.47 in group 2 and 1.25 ± 0.34 in group 3. Thus thenumber of TUNEL-positive cells in an injured spinalcord was greatly reduced by treatment with Q-VDOPh.The neurologic function scores (both the inclinedplane performance and motor grading scores) were significantlybetter in the Q-VD-OPh–treated (AU)

Introducción. En el desarrollo de daño secundario tras lesión medular están implicadas diversas caspasas.La terapia anti-caspasas ha utilizado como diana una sola caspasa que ha sido investigada en una gran variedad de estudios tanto in-vitro como in-vivo. Estos estudios han examinado el efecto neuroprotector delQ-VD-PPh, un inhibidor pan-caspasa, en un modelo delesión medular en rata. Material y métodos. Se dividieron 30 ratas Wistar entres grupos de 10 ratas cada uno: una lesión medulartraumática (con un trauma de 40 g-cm) se realizó anivel torácico grupo control (grupo 1), grupo traumacontrol (grupo 2) y el grupo de ratas tratadas con QVD-OPh (grupo 3) se realizó a nivel torácico (T8-T10) mediante la técnica de caída de peso. La respuesta a la lesión y los efectos neuroprotectores de Q-VD-OPh se valoraron mediante el examen histopatológico y la técnica de TUNEL 24 horas y 5 días tras el traumatismo. Se usó la prueba del plano inclinado de Rivlin y Tatory una versión modificada de la escala de Tarlov paravalorar el resultado funcional de las ratas 24 horas, 3 días y 5 días tras la lesión. Resultado. Veinticuatro horas tras la lesión, el estudio histopatológico de las secciones obtenidas del grupo 2 revelaron hemorragia, necrosis, trombos vasculares y edema. Las secciones obtenidos del grupo 3 mostraron hallazgos similares en ese momento. 24 horas tras lalesión el número de células apoptóticas fue 4.47 ± 0.35en el grupo 2 y 1.58 ± 0.33 en el grupo 3. Cinco días trasla lesión el número medio de células apoptóticas fue de4.35 ± 0.47 en el grupo 2 y de 1.25 ± 0.34 en el grupo 3. De esta forma el número de células TUNEL positivas enla médula dañada se redujo de forma considerable conel tratamiento con Q-VD-OPh (AU)

Calpain inhibitor AK 295 inhibits calpain-induced apoptosis and improves neurologic function after traumatic spinal cord injury in rats.

BACKGROUND: An increase in the level of intracellular calcium activates the calcium-dependent neutral protease calpain, which in turn leads to cellular dysfunction and cell death after an insult to the central nervous system. In this study, we evaluated the effect of a calpain inhibitor, AK 295, on spinal cord structure, neurologic function, and apoptosis after spinal cord injury (SCI) in a murine model. METHODS: Thirty albino Wistar rats were divided into 3 groups of 10 each: the sham-operated control group (group 1), the spinal cord trauma group (group 2), and the spinal cord trauma plus AK 295 treatment group (group 3). After having received a combination of ketamine 60 mg/kg and xylazine 9 mg/kg to induce anesthesia, the rats in groups 2 and 3 were subjected to thoracic trauma by the weight drop technique (40 g-cm). One hour after having been subjected to that trauma, the rats in groups 2 and 3 were treated with an intraperitoneal injection of either dimethyl sulfoxide 2 mg/kg or AK 295 2 mg/kg. The effects of the injury and the efficacy of AK 295 were determined by an assessment of the TUNEL technique and the results of examination with a light microscope. The neurologic performance of 5 rats from group 2 and 5 from group 3 was assessed by means of the inclined plane technique and the modified Tarlov's motor grading scale 1, 3, and 5 days after spinal cord trauma. FINDINGS: Light-microscopic examination of spinal cord specimens from group 2 revealed hemorrhage, edema, necrosis, and vascular thrombi 24 hours after trauma. Similar (but less prominent) features were seen in specimens obtained from group 3 rats. Twenty-four hours after injury, the mean apoptotic cell numbers in groups 1 and 2 were zero and 4.57 +/- 0.37 cells, respectively. In group 3, the mean apoptotic cell number was 2.30 +/- 0.34 cells, a value significantly lower than that in group 2 (P < .05). Five days after trauma, the injured rats in group 2 demonstrated significant motor dysfunction (P < .05). In comparison, the motor scores exhibited by group 3 rats were markedly better (P < .05). CONCLUSIONS: AK 295 inhibited apoptosis via calpaindependent pathways and provided neuroprotection and improved neurologic function in a rat model of SCI. To our knowledge, this is the first study to evaluate the use of AK 295, a calpain inhibitor, after SCI. Our data suggest that AK 295 might be a novel therapeutic compound for the neuroprotection of tissue and the recovery of function in patients with a SCI.