Effects of cilostazol on oxidative stress, systemic cytokine release, and spinal cord injury in a rat model of transient aortic occlusion.

BACKGROUND: Cilostazol is a phosphodiesterase inhibitor that has anti-inflammatory potential in addition to vasodilator and antiplatelet effects. The aim of this study was to determine the influence of cilostazol on biochemical markers of oxidative damage, proinflammatory cytokine release, and spinal cord injury after transient aortic occlusion in rats. METHODS: Animals were randomized into 3 groups. Sham group rats were subjected to laparotomy without aortic occlusion. Control group rats were pretreated with intraperitoneal dimethyl sulfoxide, and cilostazol group rats received intraperitoneal cilostazol (20 mg/kg/day) for 3 days before the induction of ischemia. Ischemia was induced by clamping of the infrarenal aorta, and 48 hours after reperfusion, Tarlov grades were assessed and spinal cord conduction velocities (SCCVs) were measured using epidural electrical stimulation. Erythrocyte superoxide dismutase (SOD) and catalase activities and plasma malondialdehyde, serum tumor necrosis factor-α, interleukin-1ß, and interleukin-6 levels were analyzed. Spinal cord histopathology was examined to determine neuronal damage and tissue inflammation. RESULTS: Aortic occlusion caused significant increases in SOD, catalase activities, and malondialdehyde and cytokine levels accompanied by spinal cord injury. Cilostazol significantly reduced malondialdehyde levels but did not significantly alter the activations of antioxidant enzymes, levels of proinflammatory cytokines, or histologic severity of inflammation. The differences regarding the results of Tarlov grading, SCCVs, and neuronal viability between the ischemic and cilostazol pretreated groups were statistically nonsignificant. CONCLUSION: The present experimental study indicated that cilostazol pretreatment used in this study before aortic occlusion decreased lipid peroxidation, which may be related to the reduction of reactive oxygen species. Cilostazol did not significantly suppress systemic cytokine release and prevent spinal cord inflammation and injury; however, it did show some benefit. Additional investigations might be needed to determine the critical dose of cilostazol for clarifying the protective role of this drug in spinal cord ischemia/reperfusion injury.

Adaptation of bioassay to detect endothelium-derived relaxing factors from the canine atrial endocardium.

OBJECTIVE: The aim of this study was to assess the release of endothelium-derived relaxing factors from the endocardium of canine atrial appendage. METHODS: To study the release of endothelium-derived relaxing factor (EDRF) from intact atrial endocardial endothelium, tube-shaped sutures of canine atrial appendages were performed and effluents from these tubes were bioassayed (isolated perfused organ chamber system) for detection of EDRF in canine coronary artery. RESULTS: Effluent from the right atrial appendage caused a relaxation of 58.4 +/- 10.1% and the left atrial appendage 74.9 +/- 8.5% from the initial prostagladin F2alpha contraction in coronary artery. No significant statistical difference was detected in effluent from the right and left atrial appendages. This relaxation was abolished by treating the heart tubes with Triton X-100 and reduced by treatment with LNMMA, a competitive inhibitor of nitric oxide and with indomethacin, an inhibitor of the cyclo-oxygenase pathway, also indicating the release of vasodilatory prostanoids from the endocardial endothelium. CONCLUSION: This study showed for the first time, in vitro luminal release of EDRF and prostacyclin from the canine heart atrium. The ability of the endocardial endothelium to produce these factors could play an important role in preventing thrombus formation in the cardiac chambers.

Adaptação de um sistema de ensaio biológico para detecção de fatores relaxantes endoteliais derivados do endocárdio atrial canino / Adaptation of bioassay to detect endothelium-derived relaxing factors from the canine atrial endocardium

OBJETIVO: Estudar a liberação de fatores relaxantes derivados do endotélio (EDRF) pelo endocárdio de aurículas de corações caninos. MÉTODOS: Aurículas atriais caninas foram suturadas em forma de tubos e o efluente desses tubos foram submetidos a ensaios biológicos (sistema de perfusão isolada em câmaras de órgãos) utilizando artéria coronária canina, para a detecção de EDRFs. RESULTADOS: O efluente da aurícula direita promoveu relaxamento de 58,4 + 10,1 por cento e da aurícula esquerda 74,9 + 8,5 por cento da contração inicial obtida pela ação da prostagladina F2α em artéria coronária. Não houve diferença estatística no relaxamento da artéria coronária induzido pelos efluentes das aurículas direita e esquerda. O relaxamento induzido pelos efluentes das aurículas direita e esquerda foi abolido pelo tratamento das mesmas com Triton X-100. O tratamento das aurículas com L-NMMA, um inibidor competitivo da síntese de óxido nítrico, e com indometacina, um inibidor da via da ciclooxigenase, promoveu redução no relaxamento da artéria coronária induzido pelo efluente auricular, indicando que o endotélio endocárdico libera óxido nítrico e prostanóides. CONCLUSÕES: Esse estudo demonstra, pela primeira vez, a liberação luminal in vitro de EDRF e prostaciclina pelo átrio de coração canino. A habilidade do endotélio endocárdico em produzir esses fatores pode ter um papel importante na prevenção da formação de trombos nas câmaras cardíacas.

OBJECTIVE: The aim of this study was to assess the release of endothelium-derived relaxing factors from the endocardium of canine atrial appendage. METHODS: To study the release of endothelium-derived relaxing factor (EDRF) from intact atrial endocardial endothelium, tube-shaped sutures of canine atrial appendages were performed and effluents from these tubes were bioassayed (isolated perfused organ chamber system) for detection of EDRF in canine coronary artery. RESULTS: Effluent from the right atrial appendage caused a relaxation of 58.4 + 10.1 percent and the left atrial appendage 74.9 + 8.5 percent from the initial prostagladin F2α contraction in coronary artery. No significant statistical difference was detected in effluent from the right and left atrial appendages. This relaxation was abolished by treating the heart tubes with Triton X-100 and reduced by treatment with LNMMA, a competitive inhibitor of nitric oxide and with indomethacin, an inhibitor of the cyclo-oxygenase pathway, also indicating the release of vasodilatory prostanoids from the endocardial endothelium. CONCLUSION: This study showed for the first time, in vitro luminal release of EDRF and prostacyclin from the canine heart atrium. The ability of the endocardial endothelium to produce these factors could play an important role in preventing thrombus formation in the cardiac chambers.

Comparisons of the release of vasodilator substances from left and right cardiac chambers of the isolated perfused rabbit heart: implications for intraventricular thrombus formation.

Prostacyclin (PgI(2)) and endothelium-derived nitric oxide (EDNO) are produced by the arterial and venous endothelium. In addition to their vasodilator action on vascular smooth muscle, both act together to inhibit platelet aggregation and promote platelet disaggregation. EDNO also inhibits platelet adhesion to the endothelium. EDNO and PgI(2) have been shown to be released from the cultured endocardial cells. In this study, we examined the release of vasoactive substances from the intact endocardium by using isolated rabbit hearts perfused with physiological salt solution (95% O(2)/5% CO(2), T=37 degrees C). The right and left cardiac chambers were perfused through separate constant-flow perfusion loops (physiological salt solution, 8 ml min(-1)). Effluent from left and right cardiac, separately, was bioassayed on canine coronary artery smooth muscle, which had been contracted with prostaglandin F(2alpha_)(2 x 10(-6)M) and no change in tension was exhibit. However, addition of calcium ionophore A23187 (10(-6)M) to the cardiac chambers' perfusion line induced vasodilation of the bioassay coronary ring, 61.4+/-7.4% versus 70.49+/-6.1% of initial prostaglandin F(2alpha) contraction for the left and right cardiac chambers perfusate, respectively (mean+/-SEM, n=10, p>0.05). Production of vasodilator was blocked totally in the left heart but, only partially blocked in the right heart by adding indomethacin (10(-5)M) to the perfusate, respectively, 95.2+/-2.2% versus 41.5+/-4.8% (mean+/-SEM, n=10, p<0.05). 6-Keto prostaglandin F(1alpha), measured in the endocardial superfusion effluent was also higher for the left cardiac chambers than for the right at the time of stimulation with the A23187, respectively, 25385.88+/-5495 pg/ml (n=8) versus 13,132.45+/-1839.82 pg/ml (n=8), (p<0.05). These results showed that cyclooxygenase pathway plays major role in generating vasoactive substances for the left cardiac chamber endocardium; while it is not the main pathway for the right ventricular endocardium at which EDNO and PgI(2) could act together and potentiate their antithrombogenic activities in isolated perfused rabbit heart. This may be an explanation for the intraventricular thrombus mostly seen in left ventricle rather than in right ventricle as a complication of myocardial infarction.

High-frequency ultrasonic waves cause endothelial dysfunction on canine epicardial coronary arteries.

OBJECTIVE: Application of ultrasound energy by an endarterectomy probe can facilitate the removal of atheromatous plaque, but the effect of this procedure on surrounding vessel structure and function is still a matter of experimental investigations. METHODS: To determine whether ultrasound energy impairs the production of nitric oxide or damages vascular smooth muscle function, isolated canine epicardial coronary artery segments were exposed to either high (25 W) or low (0-10 W) ultrasonic energy outputs, for 15 seconds, using an endarterectomy device prototype. After exposure, segments of epicardial coronary artery were studied in organ chambers. The following drugs were used: adenosine diphosphate (ADP), acetylcholine (Ach) and sodium fluoride (NaF) to study endothelium-dependent relaxation and sodium nitroprusside (SNP) and isoproterenol to evaluate endothelium-independent relaxation. RESULTS: Application of high ultrasonic energy power impaired endothelium-dependent relaxation to ADP (10(-9)-10(-4) M), Ach (10(-9)-10(-4) M) and NaF (0.5-9.5 mM) in epicardial coronary arteries. However, low ultrasound energy output at the tip of the probe did not alter the endothelium-dependent relaxation (either maximal relaxation or EC50) to the same agonists. Vascular smooth muscle relaxation to isoproterenol (10(-9)-10(-5) M) or SNP (10(-9)-10(-6) M) was unaltered following exposure to either low or high ultrasonic energy outputs. CONCLUSION: These experiments currently prove that ultrasonic energy changes endothelial function of epicardial coronary arteries at high power. However, ultrasound does not alter the ability of vascular smooth muscle of canine epicardial coronary arteries to relax.

Ondas ultra-sônicas de alta freqüência causam disfunção endotelial em artérias coronárias caninas epicárdicas / High-frequency ultrasonic waves cause endothelial dysfunction on canine epicardial coronary arteries

OBJETIVO: Aplicação de energia por ultra-som pode facilitar a remoção da placa ateromatosa, mas o efeito desse procedimento em vasos próximos ainda é matéria de estudos experimentais. MÉTODOS: Para determinar se a energia ultra-sônica compromete a produção de óxido nítrico, segmentos de artérias coronárias caninas foram expostos a baixos (0-10 W) e altos (25 W) níveis de energia por 15 segundos, utilizando-se protótipo de aparelho para a realização de endarterectomia. Após exposição, segmentos das artérias coronarianas foram estudados em organ chambers. Para os ensaios farmacológicos foram utilizadas as seguintes drogas:difosfato de adenosina (ADP), acetilcolina (Ach) e fluoreto de sódio (NaF) para a avaliação do relaxamento dependente do endotélio. O nitroprussiato de sódio (NPS) e o isoproterenol foram utilizados para a avaliação do relaxamento independente do endotélio. RESULTADOS: A aplicação de alta energia ultra-sônica comprometeu o relaxamento dependente do endotélio induzido por ADP (10-9 - 10-4 M), Ach (10-9 - 10-4 M) e NaF (0,5 -9,5 mM) em artérias coronarianas epicárdicas. Entretanto, baixos valores de energia ultra-sônica não alteraram o relaxamento dependente do endotélio (nem o relaxamento máximo e nem a EC50) induzido pelos mesmos agonistas. O relaxamento da musculatura lisa vascular induzido por isoproterenol (10-9 - 10-5 M) ou NPS (10-9 - 10-6 M) não foi comprometido, tanto por baixos, quanto por altos níveis de energia ultra-sônica. CONCLUSÃO: Os experimentos demonstram que altas energias ultra-sônicas alteram a função endotelial. Entretanto, o ultra-som não altera a habilidade de relaxamento da musculatura lisa vascular de artérias caninas epicárdicas.

OBJECTIVE: Application of ultrasound energy by an endarterectomy probe can facilitate the removal of atheromatous plaque, but the effect of this procedure on surrounding vessel structure and function is still a matter of experimental investigations. METHODS: To determine whether ultrasound energy impairs the production of nitric oxide or damages vascular smooth muscle function, isolated canine epicardial coronary artery segments were exposed to either high (25 W) or low (0-10 W) ultrasonic energy outputs, for 15 seconds, using an endarterectomy device prototype. After exposure, segments of epicardial coronary artery were studied in organ chambers. The following drugs were used: adenosine diphosphate (ADP), acetylcholine (Ach) and sodium fluoride (NaF) to study endothelium-dependent relaxation and sodium nitroprusside (SNP) and isoproterenol to evaluate endothelium-independent relaxation. RESULTS: Application of high ultrasonic energy power impaired endothelium-dependent relaxation to ADP (10-9 - 10-4 M), Ach (10-9 - 10-4 M) and NaF (0.5 - 9.5 mM) in epicardial coronary arteries. However, low ultrasound energy output at the tip of the probe did not alter the endothelium-dependent relaxation (either maximal relaxation or EC50) to the same agonists. Vascular smooth muscle relaxation to isoproterenol (10-9 - 10-5 M) or SNP (10-9 - 10-6 M) was unaltered following exposure to either low or high ultrasonic energy outputs. CONCLUSION: These experiments currently prove that ultrasonic energy changes endothelial function of epicardial coronary arteries at high power. However, ultrasound does not alter the ability of vascular smooth muscle of canine epicardial coronary arteries to relax.

Obesity and open-heart surgery in a developing country.

OBJECTIVE: The aim of the present study was to assess obesity as a risk of adverse outcomes following cardiac surgery. METHODS: The data of 324 consecutive patients who underwent elective procedures requiring cardiopulmonary bypass in a single cardiac center in South-Western Anatolia were retrospectively analyzed. There were 250 males and 74 females. Median age was 58.8 years (range 17 to 90 years). A body mass index (BMI)> or =30 kg/m2 was defined as obesity. Adverse outcomes analyzed included in-hospital mortality, chest tube drainage, reopening, inotropic support, arrhythmias, deep sternal wound infection, superficial surgical site infection and hospital stay duration. Multiple logistic regression analysis was performed to assess the relationship of obesity with clinical outcomes after cardiac surgery. Covariates considered in the logistic model included age, gender, pulmonary disease, cerebrovascular disease, smoking, hypertension, and diabetes. RESULTS: Fourteen percent of patients (47/324) were obese and this ratio is quite smaller than reported for industrialized countries. The results of multiple regression analysis demonstrated that obesity was a risk factor only for superficial sternal or harvesting site infection (odds ratio--4.5, 95% CI--1.404-14.679, p=0.012). CONCLUSION: Obesity was associated with increased risk of superficial surgical wound infections following cardiac surgery. In comparison with industrialized countries, obesity may account for fewer adverse events in patients undergoing open-heart surgical procedures in South-Western Anatolia, a developing country sample.

Does cardiopulmonary bypass change serum neuron-specific enolase levels?

OBJECTIVE: The effects of cardiopulmonary bypass (CPB) on serum neuron-specific enolase (NSE) levels in patients without cognitive dysfunction and neurological deficit are not yet clarified. This study was designed to see the sole effect of extracorporeal circulation on serum NSE levels in patients without any clinically observed neurological deficit. METHODS: Thirty-two consecutive patients undergoing first elective open-heart surgery were included in this prospective study. Neurological status was assessed by clinical examination before surgery, and on the postoperative first and second days. Blood samples were obtained after anesthesia induction before the administration of heparin, within the first hour post CPB, 24 and 48 hours after the end of operation. Each blood sample was assayed for hemoglobin (Hb), hematocrit and NSE levels. The Friedman's Test to compare the serial measurements of NSE and hemoglobin samples and the post-hoc Tukey test for paired comparisons between pre and postoperative values were applied Pearson correlation test was used to examine the correlation between NSE concentration and aortic cross-clamping time and CPB time, age, postoperative hematocrit and hemoglobin levels and the amount of blood products transfusion. RESULTS: There were no significant differences between NSE values at any sampling time: 11.6+/-8.0 mg/dL, 8.7+/-4.7 mg/dL, 9.3+/-5.4 mg/dL and 8.9+/-5.8 mg/dL, measured preoperatively, at the end of operation, on the first and second post-operative days, respectively. There was no significant correlation between NSE values with any of the compared variables including CPB time. CONCLUSION: This study demonstrated that the possible damage of CPB on central nervous system and on blood cells did not reach to the extent of causing any significant increase in serum NSE levels in non-complicated patients undergoing open-heart surgery.

Lipoma of the diaphragm: a rare presentation.

Lipoma of the diaphragm is an extremely rare entity. A 67-year-old asymptomatic man who had a tumor located in the posterior region of the left hemi-diaphragm is presented. The tumor was removed through a left mini-thoracotomy. The diaphragm was reconstructed primarily by using nonabsorbable suture material. The final pathologic examination revealed a mature lipoma. The patient remains without evidence of recurrence 60 months after the operation.

Is remote preconditioning as effective as direct ischemic preconditioning in preventing spinal cord ischemic injury?

BACKGROUND: Spinal cord injury remains a devastating complication of thoracic and thoracoabdominal aortic operations. The aim of this study was to assess the affectivity of direct ischemic preconditioning (PC) and remote PC in preventing spinal cord ischemic injury in an experimental model. MATERIALS AND METHODS: Thirty-eight New Zealand white rabbits were divided into five groups: One group served as Sham group (n = 7). Rabbits in other groups had their abdominal aorta cross-clamped for 40 min. Before aortic occlusion, aorta was clamped twice at the same site of aortic occlusion for 5 min followed by 15 min of reperfusion after each ischemic episode in one group (Direct PC, n = 8), left renal artery was clamped twice for 5 min followed by 15 min of reperfusion after each renal ischemic episode in one group (Remote PC, n = 8), left renal artery was first clamped for 5 min followed by 15 min of reperfusion and then aorta was clamped for 5 min followed by 15 min of reperfusion in one group (Remote + Direct PC, n = 8), and no PC method was used in Control group (n = 7). RESULTS: In all PC groups, neurological status of rabbits (Tarlov score) at post-ischemia 24th and 48th hours was better than the control group (P < 0.05), but worse than Sham group (P < 0.05). Mean viability index values in PC groups were higher than control group (P < 0.01). Post-ischemia serum NSE and MDA levels obtained in all three PC groups were significantly lower than control group (P < 0.05 and P < 0.01). CONCLUSIONS: The use of direct ischemic PC and/or remote PC is an effective way of reducing spinal cord ischemic injury because of aortic occlusion, while direct PC is more effective. The combined use of direct PC and remote PC did not provide better protection.

Effects of cyclosporin a on neurological outcome and serum biomarkers in the same setting of spinal cord ischemia model.

Spinal cord ischemic injury is one of the feared complications during aortic cross-clamping. The aim of this study was to investigate whether cyclosporin A (CsA) has a protective effect on spinal cord during ischemia in a rabbit model. A total of 22 New Zealand white rabbits were studied in three groups. One of the groups served as a sham group (n=7), in which only laparatomy was performed and closed. One group served as a control group (n=7), in which rabbits had their abdominal aortas cross-clamped for 40 min following median laparatomy. The last group was the CsA group (n=8), in which rabbits underwent the same procedure as the control group as well as CsA infusion at 20 mg/(kg . hr) over 60 min starting with aortic cross-clamping and continuing in the first 20 min of reperfusion. Neurological outcome of rabbits was evaluated according to Johnson's scale at postoperative hours 24 and 48 in all groups, and then they were killed. Their spinal cords were harvested, and segments corresponding to L4-L6 were prepared for pathological examination. Serum neuron-specific enolase (NSE) and nitric oxide (NO) levels were measured prior to and following aortic occlusion, and comparisons were made. Physiological data were similar in all groups. Rabbits in the sham group did not have any neurological deficit. However, all rabbits in the control group showed severe neurological deficits, including total paraplegia in five. According to Johnson's scale, neurological status of the rabbits at postoperative hour 48 was better in the CsA group compared to controls (p<0.01). Pathological examination of spinal cord specimens revealed a higher viability index in the CsA group compared to controls (p<0.01). Serum NSE and NO levels were lower in CsA-treated animals compared to controls. Our results demonstrate that CsA, when administered during ischemia and in the early period of reperfusion, may reduce neuronal damage in the spinal cord in a rabbit model of transient spinal cord ischemia.

Acute proximal aortic intramural hematoma: a case report.

The case presented here is of a 72-year-old man with an acute proximal aortic hematoma. He was hospitalized and underwent close monitoring and blood pressure control. Typical aortic dissection developed during his hospital admission. This case emphasizes the importance of frequent follow-up imaging during medical therapy of patients with aortic intramural hematoma. However, the frequency of imaging is yet to be determined.

Left atrial free-floating ball thrombus in a case of hyperthrophic cardiomyopathy.

Left atrial free-floating ball thrombus is a rarely seen pathology in the absence or presence of mitral valve disease. This pathologic condition carries high risks of embolic complications and deterioration of hemodynamics. The case reported here is a 34-year-old woman who had been followed-up by another center with the diagnosis of hypertrophic cardiomyopathy (HCM) was admitted to our emergency department in cardiogenic shock due to left atrial free-floating ball thrombus partially obstructed the left ventricular inflow. Emergency surgery was undertaken to remove the ball mass, additionally septal myectomy and mitral valve replacement were performed. Pathologic examination of the mass confirmed the thrombus formation. This rare case of left atrial free floating ball thrombus associated with HCM is presented and current literature is reviewed.

Myocardium utilizes more oxygen and glucose during tepid blood cardioplegic infusion in arrested heart.

The aims of this study were to evaluate myocardial metabolic activity during tepid blood cardioplegic infusion in the arrested heart in comparison with cold blood cardioplegia and to assess the early clinical outcomes of these patients. Thirty patients undergoing first elective coronary artery bypass grafting surgery were included and randomized to two groups (T for tepid and C for cold), 15 patients in each. Myocardial protection was similar in both groups except for the reinfusion of blood cardioplegia, which was 6 degrees C in group C and 28 degrees C in group T (same temperature as the body perfusion). The route of cardioplegic reinfusion was antegrade during the first reinfusion and retrograde during the second reinfusion. In order to assess myocardial metabolic activity, myocardial oxygen consumption (MVO2), myocardial glucose uptake, and myocardial lactate and acid production were all calculated. Arterial and coronary venous blood samples were obtained from the aortic root cannula and coronary sinus. During cardioplegic re-infusions in the ischemic period, the calculated values of myocardial oxygen extraction, oxygen consumption, and glucose uptake were higher in group T than in group C (P < 0.05). This difference was observed during both antegrade and retrograde delivery of cardioplegic solution. Myocardial lactate production was greater in group C than in group T during cardioplegic reinfusion, both antegradely and retrogradely (P < 0.05). In all patients, cardiopulmonary bypass was terminated in the first attempt. The clinical outcome was similar in both groups. The results of this study indicate that globally ischemic myocardium is able to utilize more oxygen and glucose during cardioplegic re-infusions at a tepid temperature in comparison to cold. In addition, the data showed evidence of less myocardial injury and better left ventricular function throughout the critical period of recovery from global ischemia for the heart protected by tepid cardioplegia.

Transpulmonary surgical closure of patent ductus arteriosus with hypothermic circulatory arrest in an adult patient.

Untreated patent ductus arteriosus carries a higher risk in adults than in children, especially when the defect is large (>4.0 mm in diameter), short, or friable. Therefore, various technical precautions have been suggested for application during surgical closure of a patent ductus arteriosus in an adult. We report the case of a 47-year-old woman with a patent ductus arteriosus who underwent transpulmonary surgical closure of the ductus under hypothermic total circulatory arrest. We discuss the technique in light of the current English-language medical literature.

Replacement of a Björk-Shiley Delrin aortic valve still functioning after 25 years.

We report the case of a patient who had undergone implantation of a Björk-Shiley Delrin valve in the aortic position 25 years earlier and who now presented with severe mitral stenosis. The patient underwent mitral valve replacement and aortic valve re-replacement. We review the justification for prophylactic replacement of Björk-Shiley Delrin heart valves.

Microalbuminuria is associated with reduced cardiac cyclic variation of integrated backscatter signal in severe hypertension.

OBJECTIVE: Microalbuminuria (MA) as a marker of systemic vascular disease and left ventricular (LV) hypertrophy is associated with increased cardiovascular mortality and morbidity in patients with essential hypertension. The aim of this study was to investigate changes in cardiac cycle-dependent variation of integrated backscatter signals (CVIBS) in hypertensive patients with MA. METHODS: Randomly selected 60 hypertensive patients (mean age 51 +/- 8) with uncontrolled blood pressure (BP) (>/=130 mmHg systolic and/or 85 mmHg diastolic) were included. All patients underwent urinary albumin excretion (UAE) measurements, 24-hour ambulatory BP monitoring, and LV echocardiographic examination. UAE was measured in two separate 24-hour urine collection and mean of two values was taken into consideration. Normotensive 20 healthy subjects served as controls. CVIBS values were obtained from mid-anteroseptal, mid-posterolateral, and mid-inferior areas at the papillary muscle level in the parasternal short-axis view. CVIBS was defined as the difference in integrated backscatter values between systole and diastole. CVIBS values in MA positive patients were compared with the values in MA negative patients and control subjects. RESULTS: Twelve patients had MA (UAE 30 to 300 mg/day) while 48 patients had normal UAE (<30 mg/day). The wall thickness (at septum and posterior) and left ventricular mass index (LVMI) values were all significantly higher in hypertensive patients with MA (P < 0.01). The CVIBS values in MA positive group were significantly lower than the CVIBS values both in MA negative hypertensive patients and control subjects (P < 0.01). CONCLUSION: This study demonstrates that in hypertensive patients a high LVMI is associated with reduced CVIBS values and MA appears to be a marker of hypertrophy.

Cyclic variation of myocardial integrated backscatter and myocardial wall thickness during percutaneous coronary angioplasty.

Cyclic variation of myocardial integrated backscatter (CVIBS) and change in myocardial wall thickness (WT%) were evaluated during percutaneous transluminal coronary angioplasty (PTCA). Fourteen patients who underwent PTCA of the proximal left anterior descending (LAD) coronary artery were included in the study. PTCA was performed by inflating the balloon at the site of the LAD lesion for 1 minute. CVIBS was measured at three episodes during PTCA in the parasternal short-axis view: before the inflation, at the end of 1-minute inflation, and at the fifth-minute after deflation of the balloon. Three regions of interest were used to evaluate the three-vessel territories: mid-anteroseptal area for LAD, mid-posterolateral area for circumflex artery, and mid-inferior area for right coronary artery. The WT% was calculated in each area. In the LAD territory, CVIBS measured at the end of 1-minute inflation was lower than the values obtained before PTCA, 5.2 +/- 1.0 decibel (dB) versus 3.7 +/- 0.7 dB (P < 0.01). CVIBS magnitudes increased at the fifth-minute after the deflation back up even to higher levels than pre-PTCA values,6.1 +/- 1.0 dB versus 5.2 +/- 1.0 dB (P < 0.01). The WT% values decreased during balloon inflation but did not recover to the pre-inflation values measured at fifth-minute after deflation. In other sites, there was no change in either CVIBS or WT% values at any time studied. The observed increase in CVIBS may be an indicator of restoration of blood flow to ischemic myocardium.

Novel approach to measure myocardial performance index: pulsed-wave tissue Doppler echocardiography.

A simple, reproducible, noninvasive myocardial performance index (MPI) for the assessment of overall cardiac function has been described previously. The purpose of this study was to compare the MPI obtained by pulse Doppler method with the MPI obtained by tissue Doppler echocardiography (TDE) in normal subjects and patients with dilated cardiomyopathy (DCMP). Fifteen patients with DCMP and 15 healthy subjects were included. In order to calculate MPI by TDE, isovolumetric contraction (IVCT), relaxation time (IVRT), and ejection time (ET) were measured at two different sites of mitral annulus: septum and lateral. MPI was calculated by dividing the sum of IVCT and IVRT by ET at each site of measurement. The mean MPI value was found by dividing the sum of these MPI values into two. The same parameters were measured using the mitral inflow and left ventricular outflow velocity time intervals in pulsed Doppler method. At all sites measured, MPI by TDE correlated well with conventional MPI both in healthy subjects and patients with DCMP. The highest correlation was observed in mean values of MPI by TDE:r = 0.94, P < 0.0001in healthy subjects; andr = 0.95, P < 0.0001in patients with DCMP. In conclusion, this study clearly demonstrated that MPI could be measured by TDE and it correlated well with conventional MPI in normal and diseased heart.

Value of measuring myocardial performance index by tissue Doppler echocardiography in normal and diseased heart.

Myocardial performance index (MPI) is a simple and reproducible method for the assessment of overall cardiac function. In this study, we evaluated the applicability and usefulness of pulsed-wave tissue Doppler echocardiography (TDE) as a tool to calculate MPI in comparision with a conventional Doppler method. Twenty-five patients with previous myocardial infarction (MI) and 15 healthy subjects were included. In order to calculate MPI by TDE, isovolumetric contraction time (IVCT), isovolumetric relaxation time (IVRT), and ejection time (ET) were measured at four different sites in the mitral annulus: septum, lateral, anterior, and inferior. MPI was calculated by dividing the sum of IVCT and IVRT by ET at each site of measurement. The mean MPI value was found by dividing the sum of these MPI values into four. The same parameters were measured using the mitral inflow and left ventricular outflow velocity time intervals by a conventional method. MPI by TDE correlated well with conventional MPI in healthy subjects (r = 0.81, P < 0.0001). Although it continued to be statistically significant, the correlation between the two methods of measuring MPI, TDE and conventional, in patients with previous MI was not as high as it was in healthy individuals (P < 0.001, r = 0.62). This is due to the lesser degree of correlation between IVRT and IVCT values obtained by TDE and the conventional method (r = 0.49, P < 0.05; r = 0.56, P < 0.05; respectively). In conclusion, this study has demonstrated that MPI could be measured by tissue Doppler and that it correlated well with conventional MPI. Moreover, MPI by TDE has the advantage of assessing both regional and global myocardial performance.