An easy method for monitoring patients with pulmonary Hypertension: P-wave dispersion.

BACKGROUND: Pulmonary arterial hypertension (PAH) is a haemodynamic and pathophysiological condition with restricted flow through the pulmonary arterial circulation. In pulmonary hypertension, right ventricular hypertrophy and diastolic dysfunction can lead to an increase in atrial strain, fibrosis and dilation, which cause inhomogeneous atrial conduction. Interlead variation in P-wave duration is called P-wave dispersion (PwD), which is an electrocardiographic parameter that can be used to predict atrial arrhythmias. Our aim was to investigate the relationship between PwD, functional capacity, and invasive and non-invasive haemodynamic parameters of patients diagnosed with PAH. METHODS: Between 2015 and 2017 we enrolled 33 patients admitted to our in-patient clinic and diagnosed with PAH, and 32 healthy individuals for the control group. Details of these patients at the time of diagnosis were analysed, including gender, age, physical examination, electrocardiogram (ECG), echocardiography, six-minute walk test distance (6MWD), haemodynamic parameters and blood tests for biochemical markers that are correlated with clinical severity. Statistical analyses were performed using SPSS version 20.0 (SPSS Inc, Chicago, Illinois, USA). Statistical significance was taken as p < 0.05. RESULTS: In the forward stepwise multiple linear regression analysis, PwD and mean pulmonary artery pressure determined by right heart catheterisation were independently related to the functional capacity tested by the 6MWD (p < 0.02 and p < 0.01, respectively). CONCLUSIONS: PwD can easily be calculated from a surface ECG to indirectly estimate the functional status and prognosis of the patient with PAH.

Blood pressure control in anticoagulated hypertensive patients.

OBJECTIVE: To compare the methods of office blood pressure (BP) measurement and ambulatory blood pressure monitoring (ABPM) to ensure optimal BP control in hypertensive anticoagulated patients. PATIENTS AND METHODS: Seventy-eight patients who were receiving antihypertensive drugs and warfarin in a dose-adjusted approach to achieve therapeutic international normalized ratio because of the association of atrial fibrillation were enrolled in the study. Twenty-four hour ABPM was applied to all patients. For the assessment of optimal BP control, office BP measurements were compared with ABPM recordings. All patients were divided into 'good control' and 'poor control' groups with a cut-off level of 140 mmHg systolic blood pressure (SBP). The groups of patients with 'good control' and 'poor control' were further subdivided into four groups according to the cardiovascular outcome on the basis of ABPM reference threshold levels: 'true good control' or 'seemingly good control' and 'true poor control' or 'seemingly poor control' (white coat effect). Positive and negative predictive values of the office BP measurement method versus ABPM were estimated. RESULTS: According to office measurements, 56.9% of all cases were in the 'good control' group and 43.1% were in the 'poor control' group. When we reclassified patients according to daytime and night-time mean SBP, we realized that they were in 'true good control', 'seemingly good control', 'true poor control', and 'seemingly poor control' groups with ratios of 25.5, 31.4, 21.6, and 21.6% on the basis of daytime systolic mean values and 19.6, 37.3, 35.3, and 7.8% on the basis of night-time systolic mean values, respectively. When we considered ABPM as a reference method, sensitivity, specificity, and positive and negative predictive values of office SBP measurements were 40.74, 54.17, 50.00, and 44.83% for daytime SBP mean values and 48.65, 71.43, 81.82, and 34.48% for night-time SBP mean values, respectively. CONCLUSION: Poor control of SBP in patients with anticoagulant therapy may result in fatal events such as intracranial bleeding; thus, they are still under significant risk, although they are considered to have controlled BP with office measurements. ABPM is an essential method for accurate BP control in contrast to office BP measurement in anticoagulated patients.

Baseline SYNTAX score and long-term outcome in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention.

OBJECTIVES: The SYNTAX score (SXscore) has emerged as a reproducible angiographic tool to quantify the extent of coronary artery disease based on the location and complexity of each lesion. The aim of this study was to evaluate whether the SXscore is an independent predictor of long-term cardiovascular outcomes in patients treated with primary percutaneous coronary intervention (PCI) for acute ST-segment elevation myocardial infarction (STEMI). METHODS: A total of 2993 patients with acute STEMI who underwent primary PCI were stratified into the 4 groups according to the SXscore quartiles; quartile 1(Q1, SXscore ≤ 9, n = 819), Q2 (9 < SXscore < 16, n = 715), Q3 (16 ≤ SXscore < 20, n = 710), and Q4 (SXscore ≥ 20, n = 749). RESULTS: There were significant differences among the quartiles with respect to age, basal creatinine and glucose levels, and the incidences of diabetes mellitus, Killip ≥2, and anemia. From Q1 to Q4, there were increasing rates of culprit left anterior descending lesion (P < .001), multivessel disease (P < .001), chronic total occlusion (P < .001), and proximal lesion localization (P < .001). At long-term follow-up, all-cause mortality, nonfatal myocardial infarction, stroke, rehospitalization due to heart failure, and the need of revascularization were significantly more frequent among the patients in the highest SXscore quartile. In multivariate analysis, after including the SXscore as a numerical variable into the model, every point of increase was determined as an independent predictor for long-term mortality (hazard ratio [HR] 1.03, 95% confidence interval [CI] 1.01-1.05, P = .008) and for overall major adverse cardiac events (MACEs; HR 1.02, 95% CI 1.01-1.04, P < .001). CONCLUSION: The SXscore is an independent predictor of both in-hospital and long-term mortality and MACE in patients with acute STEMI undergoing primary PCI.

The effects of endothelial lipase gene (LIPG) variants on inflammation marker levels and atherosclerosis development.

Atherosclerosis is a major pathological process related with several important adverse vascular events including coronary artery disease, stroke, and peripheral arterial disease. Endothelial lipase is an enzyme the activity of which affects all of lipoproteins, whereas HDL is the main substrate. The purpose of our study was to investigate the effects of endothelial lipase gene polymorphism and inflammation markers (CRP, IL-1ß, IL-6, IL-8 and TNF-α) in the atherosclerosis. 104 patients with atherosclerosis and 76 healthy individuals were included in the study. LIPG -584C/T polymorphism gene polymorphisms were assessed with PCR-RFLP method. The serum CRP levels were measured by turbidimetric method using a biochemistry autoanalyzer, whereas serum IL-1ß, IL-6, IL-8, TNF-α levels were determined by enzyme-linked immunosorbent assay. In this study, we found that the frequencies of TC genotype are more prevalent in patients than controls. We found a statistically significant difference of IL-6 levels between patient and control group. Our findings suggest that T allele might play a potential role in the susceptibility to atherogenesis in the Turkish population.

[Reshaping the left Judkins catheter for a right coronary angiogram in the anomalous aortic origin of the right coronary: killing two birds with one left Judkins]. / Sag koroner arter çikis anomalilerinde yeniden sekillendirilen sol Judkins kateter ile sag koroner anjiyografisi: Bir sol Judkins ile iki kus

OBJECTIVES: Selective cannulation of the right coronary artery (RCA) in the anomalous aortic origin of the RCA is technically difficult and challenging. In this study, we tested the success of RCA cannulation with a reshaped left Judkins catheter in cases of difficult selective cannulation. STUDY DESIGN: The study population consisted of 837 consecutive patients (456 male, 381 female) that were admitted to our hospital with stable angina pectoris and acute coronary syndrome between October 1 and December 31, 2011. In cases where RCA cannulation was difficult, the 10 centimeter section of the left Judkins proximal to the secondary curve was reshaped by hand to form an inward slope. The secondary curve angle was increased to approximately 100 degrees and the primary curve angle was adjusted to 120 degrees. Then, we attempted to perform selective RCA cannulation. RESULTS: In 49 of the 837 patients, selective RCA cannulation was unsuccessful with the right Judkins catheter. In 42 of these 49 (86%) cases, the RCA was cannulated with the reshaped left Judkins. We failed to cannulate the right coronary in two cases with downward angulation, one with upward angulation, one with high take-off origin, and one with anterior origin. A multipurpose, internal mammary artery, left Amplatz 1, and right Amplatz 1 catheter were used for cannulation in these cases, respectively. There was no angina, nor were there electrocardiographic or hemodynamic changes during the procedure. CONCLUSION: In cases where the selective cannulation of the RCA is difficult, using a reshaped left Judkins may be a successful and cost-effective method of selective cannulation.

Measurement of the coronary flow velocity reserve in patients with non-alcoholic fatty liver disease.

BACKGROUND/AIMS: Endothelial dysfunction is an early and reversible feature in the pathogenesis of atherosclerosis. Coronary flow velocity reserve is a noninvasive test showing endothelial function of epicardial coronary arteries and coronary microcirculatory function. This study was designed to evaluate the carotid intima-media thickness and myocardial microvascular circulation in patients with non-alcoholic fatty liver disease. MATERIALS AND METHODS: Twenty-four patients with non-alcoholic fatty liver disease and 28 healthy subjects were studied. According to the pathology of liver biopsies, patients with non-alcoholic fatty liver disease were divided into non-alcoholic fatty liver and nonalcoholic steatohepatitis groups. Coronary diastolic peak flow velocities were measured at baseline, and then dipyridamole infusion was measured by transthoracic Doppler echocardiography. The ratio of hyperemic to baseline diastolic peak velocities was calculated and the intima-media thicknesss of the carotid arteries were measured. RESULTS: Baseline average diastolic peak and diastolic mean flow velocities were similar between non-alcoholic fatty liver disease patients and healthy subjects. However, hyperemic average diastolic peak and diastolic mean flow velocities were significantly lower in the patient groups compared to those in the controls (p=0.005 and p=0.002). Coronary flow velocity reserve was 1.65 ± 0.36 and 2.67 ± 0.81 in patients and healthy subjects, respectively (p < 0.001). The intima-media thickness was similar between the patients with non-alcoholic fatty liver disease and healthy subjects. The comparison of patients with non-alcoholic fatty liver and non-alcoholic steatohepatitis within the non-alcoholic fatty liver disease group with respect to coronary flow velocity reserve and intima-media thickness yielded no statistical differences. CONCLUSIONS: The present study showed that coronary flow velocity reserve, which establishes coronary microvascular and endothelial functions noninvasively, is significantly impaired in patients with non-alcoholic fatty liver disease. The impaired coronary flow velocity reserve-like early atherosclerotic changes may have value in the prediction of coronary artery disease in patients with non-alcoholic fatty liver disease.

Effect of cigarette smoking on platelet aggregation.

BACKGROUND: Cigarette smoking may increase platelet aggregation and cause atherothrombotic cardiovascular events. We aimed to investigate the impact of cigarette smoking on platelet function in patients with ischemic coronary heart disease (CHD). METHODS: Twenty patients with ischemic stable CHD under aspirin therapy (300 mg/d), who continue to smoking despite all warnings, and 20 nonsmokers with CHD are enrolled in the study. Platelet function is studied at the morning, before and 15 minutes after the first cigarette, by the Platelet Function Analyzer (PFA)-100, with collagen and epinephrine and collagen and adenosine diphosphate cartridges. Post aspirin platelet hyperactivity is defined as having a closure time (CT) shorter than 186 seconds despite regular aspirin intake. Serial CT measurements are analyzed by paired samples t test. RESULTS: Persistent platelet activity was present in 4 smoker (20%) and 3 nonsmoker (15%) patients at the beginning. Platelet activity measured by the PFA-100 is been increased significantly after cigarette smoking (P = .004). Shorter CTs were determined after smoking in all patients with and without baseline persistent platelet activity, and 4 more participants became aspirin nonresponder (P = .004). No significant differences in demographic, hematological, and biochemical parameters were determined between aspirin responders and nonresponders. CONCLUSIONS: We determined that cigarette smoking may increase platelet aggregation in patients with ischemic CHD in an aspirin nonresponsive manner. Our results emphasize the importance of quitting cigarette smoking in patients with CHD.

The accuracy of deceleration time of diastolic coronary flow measured by transthoracic echocardiography in predicting long-term left ventricular infarct size and function after reperfused myocardial infarction.

AIMS: Assessment of microvascular function after reperfused acute myocardial infarction (AMI) provides important insights for myocardial reperfusion and facilitates prediction of long-term left ventricular (LV) function and clinical outcome. In this study, we examined microvascular integrity 48 h after successful primary percutaneous coronary intervention (PCI) and compared predictive accuracy of the intracoronary pressure-wire- and transthoracic Doppler echocardiography-based parameters in the estimation of long-term LV infarct size and function. METHODS AND RESULTS: The study group consisted of 30 anterior AMI patients who were treated successfully with primary PCI. Two days after primary PCI, microvascular integrity was evaluated. Coronary flow reserve (CFR), collateral flow index (CFIp), coronary wedge pressure (CWP), and index of microvascular resistance (IMR) were determined using intracoronary pressure wire. Deceleration time of coronary diastolic flow (DDT) was measured using transthoracic echocardiography. At 6 months, coronary angiography, echocardiography, and infarct size measurement were performed. Area under the curve, sensitivity, and specificity of the indices of microvascular perfusion in the prediction of late-term infarct size were as follows: IMR (0.68 ± 0.15, 69%, 60%), CFR (0.67 ± 0.10, 66%, 59%), CWP (0.69 ± 0.12, 70%, 72%), CFIp (0.64 ± 0.10, 65%, 78%), and DDT (0.68 ± 0.16, 69%, 79%). All of the microvascular perfusion indices, which have been used in this study, had comparable sensitivity and specificity in the prediction of long-term ejection fraction. There were no significant differences between areas under the curve of microvascular perfusion indices in the prediction of long-term infarct size and ejection fraction. CONCLUSION: As a non-invasive parameter, DDT was found to be as accurate as the invasive parameters of microvascular function in estimating long-term infarct size and LV function. Thus, simply measuring DDT in the reperfused infarct-related artery might provide useful and reliable estimate for early risk stratification.

Concurrent microvascular and infarct remodeling after successful reperfusion of ST-elevation acute myocardial infarction.

BACKGROUND: Connection between the course of microvascular and infarct remodeling processes over time after reperfused ST-elevation acute myocardial infarction has not been fully elucidated. The aim of this study is to investigate the association of temporal changes in hemodynamics of microcirculation in the infarcted territory and infarct size (IS) after primary percutaneous coronary intervention in patients with ST-elevation acute myocardial infarction. METHODS AND RESULTS: Thirty-five patients admitted with ST-elevation acute myocardial infarction undergoing primary percutaneous coronary intervention were enrolled in the study. Coronary flow reserve (CFR), index of microvascular resistance (IMR), and IS were assessed 2 days after primary percutaneous coronary intervention and at the 5-month follow-up. The predictors of the 5-month IS were the baseline values of IS (beta=0.6, P<0.001), IMR (beta=0.280, P=0.013), and CFR (beta=-0.276, P=0.017). There were significant correlations between relative change in IS and relative change in measures of microvascular function (IS and CFR [r=-0.51, P=0.002]); IS and IMR ([r=0.55, P=0.001]). In multivariate model, relative changes in IMR (beta=0.552, P=0.001) and CFR (beta=-0.511, P=0.002) were the only predictors of relative change in IS. In patients with an improvement in IMR >33%, the mean IS decreased from 32.3+/-16.9% to 19.3+/-14% (P=0.001) in the follow-up. Similarly, in patients with an improvement in CFR >41%, the mean IS significantly decreased from 29.9+/-20% to 15.8+/-12.4% (P=0.003). But in patients with an improvement in IMR and CFR, which were below than the mean values, IS did not significantly decrease during the follow-up. CONCLUSIONS: Improvement in microvascular function in the infarcted territory is associated with reduction in IS after reperfused ST-elevation acute myocardial infarction. This link suggests that further investigations are warranted to determine whether therapeutic protection of microvascular integrity results in augmentation of infarct healing.

Improvement of coronary flow velocity reserve with telmisartan in patients with autosomal-dominant polycystic kidney disease.

OBJECTIVES: Endothelial dysfunction (ED) has been reported in patients with autosomal-dominant polycystic kidney disease (ADPKD). Coronary flow velocity reserve (CFVR) is a noninvasive test showing endothelial function of epicardial coronary arteries and coronary microcirculatory function. The aim of this study was to investigate the effect of the angiotensin receptor blocker, telmisartan, on CFVR in patients with ADPKD. METHODS: Thirteen patients with ADPKD and well-preserved renal function and 22 healthy controls were included in the study. CFVR was measured at baseline and after dipyridamole infusion by echocardiography. CFVR was calculated as the ratio of hyperemic to baseline average peak diastolic velocities. After the baseline evaluation of CFVR, patients started telmisartan at a dose of 80 mg/day and were followed for 12 months. CFVR was remeasured after 6 and 12 months of therapy. RESULTS: Patients with ADPKD had significantly lower CFVR compared to healthy subjects. CFVR increased significantly after 6 months and 12 months of telmisartan therapy (P = 0.001) in patients with ADPKD. CONCLUSION: One year of telmisartan therapy significantly improved CFVR in patients with ADPKD. This finding suggests that the stimulation of the renin-angiotensin-aldosterone system contributes to the ED in these patients.

Endothelial dysfunction in hemodialysis patients with failed renal transplants.

BACKGROUND: Endothelial dysfunction (ED) is a common precursor and denominator of cardiovascular events including development of atherosclerosis. In this cross-sectional study, we aimed to investigate ED, measured by coronary flow reserve (CFR) in hemodialysis (nHD) patients who were never transplanted and patients with failed renal transplants restarting hemodialysis (fTx-HD). METHODS: Forty nHD (24 males, mean age 39 ± 9 yr) and 43 fTx-HD patients (27 males, mean age 36 ± 9 yr) were included in the study. Clinical and biochemical parameters, including high-sensitive C-reactive protein (hs-CRP) levels were determined. Also, CFR measurements were used to evaluate ED. RESULTS: There were no significant differences regarding age, gender, smoking status, systolic and diastolic blood pressure levels, mean duration of HD treatment as well as Kt/V((urea)) values between the two groups. Time spent on dialysis in the nHD group and dialysis duration following failure of renal allograft in the fTx-HD group were similar. Serum creatinine, hemoglobin, hematocrit, calcium and phosphorus levels were similar between the two groups as well. When compared to nHD group, serum total cholesterol (139 ± 3 vs. 154 ± 3 mg/dL, p = 0.045), serum albumin (3.8 ± 0.3 g/dL vs. 4.1 ± 0.2 g/dL, p < 0.0001) and CFR (1.60 ± 0.2 vs. 1.75 ± 0.3, p = 0.028) levels were significantly lower, while serum hs-CRP levels (11 ± 15 mg/L vs. 3 ± 4 mg/L, p = 0.001) were significantly higher in the fTx-HD group. Serum hs-CRP negatively correlated (r = -0254, p = 0.021), while serum albumin positively correlated (r = 0402, p = 0.001) with CFR values. CONCLUSION: ED is more prominent in fTx-HD than the nHD patients. Inflammation, caused by failed renal allograft can be responsible for this abnormality.

Infarct remodeling process during long-term follow-up after reperfused acute myocardial infarction.

BACKGROUND: After acute myocardial infarction (AMI), the recovery of perfusion in infarct area may lead to significant spontaneous infarct size (IS) reduction during the subsequent period. The natural course of infarct-healing process after reperfusion therapy has not been fully elucidated. In this study, we investigated the time course of the spontaneous infarct-healing process in patients with reperfused AMI. METHODS AND RESULTS: Fifty-two patients with AMI who underwent primary percutaneous intervention were included. IS was measured with single-photon emission tomography using Bull's eye method at 4th day, at 5th, and at 10th months. IS was expressed as a percentage of the total myocardium. IS decreased by 33.6% at 5th month when compared with 4th day IS (from 26.3% +/- 18.8% to 17.5% +/- 12.9%, P < 0.001, n = 44). At 10th month, mean IS decreased by 21% when compared with 5th month IS (from 15.89% +/- 12.65% to 12.53% +/- 9.35%, P = 0.007, n = 31) and 49% when compared with 4th day IS (24.02% +/- 17.67% to 12.53% +/- 9.35%, P < 0.001). CONCLUSION: Significant endogenous recovery of perfusion in the infarct area occurs at the long term in patients with reperfused AMI. Infarct healing is a dynamic and ongoing process and decrease in IS continues long term after reperfused AMI.

Effect of intracoronary streptokinase administered immediately after primary percutaneous coronary intervention on long-term left ventricular infarct size, volumes, and function.

OBJECTIVES: The purpose of this study was to investigate the reflections of the improvement in microvascular perfusion provided by adjuvant intracoronary streptokinase (ICSK) on late-phase infarct size and left ventricular volumes and functions. BACKGROUND: It has been shown that ICSK given immediately after primary percutaneous coronary intervention (PCI) improves myocardial perfusion in the early days of ST-segment elevation acute myocardial infarction. METHODS: Ninety-five patients undergoing primary PCI were randomized to ICSK 250 kU (n = 51) or no additional therapy (n = 44). Two days later, coronary hemodynamic indexes were measured to evaluate tissue-level perfusion. After 6 months, angiography, echocardiography, and technetium-99m single-photon emission computed tomography (SPECT) were performed. RESULTS: At 2 days, all indexes of microvascular function were significantly better in the ICSK group than in the control group, including coronary flow reserve (2.5 vs. 1.7, p < 0.001) and index of microvascular resistance (20.2 vs. 34.2, p < 0.001). At 6 months, infarct size (22.7% vs. 32.9%; p = 0.003) and left ventricular end-systolic (41.1 ml vs. 60.9 ml; p = 0.009) and end-diastolic volumes (95.5 ml vs. 118.3 ml; p = 0.006) were significantly smaller, and the ejection fraction was significantly higher (57.2% vs. 51.8%; p = 0.018) in the ICSK group compared with the control group. CONCLUSIONS: In this study, it has been demonstrated that low-dose ICSK given immediately after primary PCI significantly limits long-term infarct size and preserves left ventricular volumes and functions. (Effect of Complementary Intracoronary Streptokinase Administration Immediately After Primary Percutaneous Coronary Intervention on Microvascular Perfusion and Late Term Infarct Size in Patients With Acute Myocardial Infarction; NCT00302419).

Rosai-Dorfman disease with factor XII deficiency.

A 17-year-old female patient presented with chronic symmetrical oligoarthritis of both knees and ankles, xerostomia, xerophthalmia, multiple bilateral lymphadenopathies in the cervical region, and bilateral parotid enlargement with the histological finding of chronic sialoadenitis. She had been already given methotrexate, chloroquine, and corticosteroids with the diagnosis of rheumatoid arthritis (RA) before referral to our outpatient clinic. Because her complaints and the lumps did not remit and she could be classified as neither RA nor primary Sjögren's syndrome (SS) according to 1987 ACR RA criteria or European preliminary criteria for SS, lymph node biopsy was repeated and revealed the diagnosis of Rosai-Dorfman disease (RDD) with the histological findings of histiocytes, phagocyting lymphocytes in enlarged sinuses, and mature plasma cells infiltrating the pulpa. All the medications were stopped after the pathological diagnosis of RDD and consulting with the Division of Hematology. She was reevaluated with magnetic resonance imaging, which showed dense infiltrative areas around knee and ankle joints, and computed tomography that showed a soft tissue mass surrounding the descending aorta and upper part of the abdominal aorta. Activated partial thromboplastin time was found to be prolonged in prebiopsy examinations, and factor XII deficiency was detected after detailed hematological evaluation. The symptoms of joint involvement were relieved with nonsteroidal antiinflammatory drugs. She has been followed-up without medication without obvious clinical or laboratory change. We herein report a patient with RDD mimicking RA and SS. We consider that RDD should be kept in mind especially in patients with resistant symptoms to conventional therapies, younger disease onset, and predominant parotid and lymph node enlargement.

Coronary flow reserve dysfunction in hemodialysis and kidney transplant patients.

BACKGROUND: The assessment of coronary flow reserve (CFR) by trans-thoracic echocardiography has recently been introduced into clinical studies. Impairment of coronary microvascular functions and decreased CFR detected by trans-thoracic Doppler harmonic echocardiography (TTDE) has recently been reported in hemodialysis (HD) patients, but there is no comparative study between HD patients and renal transplant recipients. METHODS: The aim of our study was to evaluate coronary microvascular circulation in chronic HD patients and renal transplant recipients. Forty-eight chronic HD patients, 27 renal transplant patients and 39 normotensive healthy controls were studied for the assessment of CFR by TTDE. The carotid artery intima media thickness (IMT) and areas of focal plaque formation were also evaluated in all subjects. RESULTS: CFR values were significantly lower in both the HD and renal transplant groups than in the control group (p = 0.00). CFR values (1.57 +/- 0.32 vs. 1.89 +/- 0.50, p = 0.01) were also significantly lower in the HD group than in the renal transplant group. In 43 of 48 (89.6%) HD patients, CFR was <2.0; however, in 16 of 27 (59.3%) renal transplant recipients it was <2.0 (p = 0.00). When the HD and renal transplant groups were divided into two subgroups, according to CFR measurements (CFR < 2 and > or =2), no significant differences were found with respect to coronary risk factors and left ventricular echocardiographic measurements. The IMT of the control group (0.586 +/- 0.163 mm) was significantly lower than the HD (0.799 +/- 0.218 mm) and renal transplant groups (0.681 +/- 0.148 mm; p = 0.00). The IMT of the HD patients (0.799 +/- 0.218 mm) was significantly higher than the renal transplant recipients (0.681 +/- 0.148 mm; p = 0.01). CONCLUSIONS: Renal transplant and HD patients had lower CFR values detected by TTDE, which may be regarded as an early finding of an affected cardiovascular system. CFR is more impaired in HD patients than renal transplant recipients. Uremia-associated microvascular disease may be responsible for CFR impairment in HD patients.

Reduced coronary flow reserve and early diastolic filling abnormalities in patients with nephrotic syndrome.

BACKGROUND: Increased cardiovascular disease risk is very well known in nephrotic syndrome. Coronary flow reserve measurement by trans-thoracic echocardiography reflects coronary microvascular and endothelial function. However, diastolic filling abnormalities by echocardiography may indicate diastolic dysfunction. Our aim was to evaluate endothelial and diastolic functions by trans-thoracic echocardiography in nephrotic syndrome. METHODS: Eighteen patients with nephrotic syndrome (five females, 34 +/- 17 years) and 30 controls (10 females, 35 +/- 10 years) were evaluated in this cross-sectional observational study. Age, weight, lipid profile, glucose, blood urea nitrogen, creatinine, serum albumin, total protein, C-reactive protein, erythrocyte sedimentation rate, blood pressures, 24-hour urine volume, and protein were recorded. Glomerular filtration rate was estimated by Cockcroft-Gault Formula. Doppler flow and other echocardiographic parameters were measured by Vivid 7 echocardiography. RESULTS: Coronary flow reserve was significantly lower in patients than controls (p < 0.001) and was negatively correlated with proteinuria (p < 0. 001), creatinine levels (p = 0.03), total cholesterol (p = 0.02), C-reactive protein (p = 0.02), and erythrocyte sedimentation rate (p = 0.005). E/A ratio was significantly lower in patients than in controls (p = 0.005). DT was significantly higher in patients than in controls (p = 0.01) and isovolumic relaxation time was similar in both groups. CONCLUSION: Coronary flow reserve and left ventricular diastolic filling are significantly impaired in nephrotic syndrome. Proteinuria, serum creatinine, total cholesterol and inflammation may have all contributory effects on endothelial dysfunction. Early evaluation of patients with nephrotic syndrome should include coronary flow and diastolic function by echocardiography.

Coronary flow velocity reserve and carotid intima media thickness in patients with autosomal dominant polycystic kidney disease: from impaired tubules to impaired carotid and coronary arteries.

BACKGROUND AND OBJECTIVES: Cardiovascular problems are a major cause of morbidity and mortality in patients with autosomal dominant polycystic kidney disease. Endothelial dysfunction, an early and reversible feature in the pathogenesis of atherosclerosis, is associated with increased vascular smooth muscle tone, arterial stiffening, and increased intima-media thickness. Coronary flow velocity reserve is a noninvasive test showing endothelial function of epicardial coronary arteries and coronary microcirculatory function. The aim of the study was to investigate the carotid intima-media thickness and coronary flow velocity reserve in patients with autosomal dominant polycystic kidney disease. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Thirty normotensive patients with autosomal dominant polycystic kidney disease (10 male, 20 female) with well-preserved renal function and 30 healthy subjects (12 male, 18 female) were included in the study. Coronary flow velocity reserve was measured at baseline and after dipyridamole infusion by echocardiography. Coronary flow velocity reserve was calculated as the ratio of hyperemic to baseline diastolic peak velocities. RESULTS: Carotid intima-media thickness was significantly higher in patients than in control subjects (0.80 +/- 0.29 versus 0.54 +/- 0.14 mm, respectively; P < 0.001). Moreover, coronary flow velocity reserve was significantly lower in patients than in control subjects (1.84 +/- 0.39 versus 2.65 +/- 0.68, respectively; P < 0.001). CONCLUSIONS: Normotensive patients with autosomal dominant polycystic kidney disease with well-preserved renal function have significantly increased carotid intima-media thickness and significantly decreased coronary flow velocity reserve compared with healthy subjects. These findings suggest that atherosclerosis starts at an early stage in the course of their disease in patients with autosomal dominant polycystic kidney disease.

Acute effects of smoking on coronary flow velocity reserve and ventricular diastolic functions.

Although it is well known that chronic effect of smoking on cardiovascular system, relation between coronary vascular reactivity and ventricular functions after acute smoking has not been well understood. The purpose of this study was to assess the relation between coronary flow velocity reserve and ventricular diastolic functions measured by tissue Doppler imaging after acute smoking. We found that coronary flow velocity and diastolic functions of right ventricle were decreased. Also, there was a correlation between coronary flow velocity reserve and diastolic ratio of the ventricle. Acute smoking may affect diastolic functions of the ventricles, especially right ventricle via changes of coronary flow.

Coronary flow reserve is impaired in patients with adult growth hormone (GH) deficiency.

OBJECTIVE: Relationship between adult growth hormone deficiency (AGHD) and increased cardiovascular disease risk is very well known in hypopituitary patients treated with conventional hormone replacement therapy other than growth hormone (GH) administration. Endothelial dysfunction, an early and reversible event in pathogenesis of atherosclerosis, is associated with increased vascular smooth muscle tone, arterial stiffening and intima-media thickness (IMT). Coronary flow reserve (CFR) measurement by transthoracic Doppler echocardiography (TTDE) reflects coronary microvascular and endothelial functions, as a cheaper and an easy screening test. We have used TTDE to evaluate endothelial function and coronary microvascular function in AGHD. DESIGN: Cross-sectional observational study. PATIENTS: A total of 10 GH-deficient adults on conventional replacement therapy other than GH (4 males, 6 females; mean age 37 +/- 11 years) and 15 healthy subjects (7 males, 8 females; mean age 41 +/- 11 years) were studied. Patients and controls were all nonsmokers, normotensive and nondiabetic. MEASUREMENTS: IGF-1, free T4, lipid profile, insulin, glucose, insulin resistance (IR), anthropometrical and physical parameters were recorded. CFR recordings and IMT measurements were performed using the Vivid 7 echocardiography device. RESULTS: IMT were significantly higher in patients than controls (0.70 + 0.19 mm and 0.53 + 0.13 mm, respectively; P = 0.02). CFR was significantly lower in patients than in controls (1.96 +/- 0.35 and 2.62 +/- 0.45, respectively; P < 0.001). CFR was positively correlated with IGF-1 levels (r = 0.54, P = 0.005). CONCLUSION: CFR is significantly lower in adults with GH deficiency than in controls. Direct correlation between CFR and IGF-1 concentrations suggests GH replacement could improve microvascular function and thereby could decrease cardiovascular morbidity and mortality in AGHD.