Atherosclerosis and vascular calcification are independent predictors of left ventricular hypertrophy in chronic haemodialysis patients.

BACKGROUND: Accelerated atherosclerosis and vascular calcification are common in chronic haemodialysis (HD) patients. In this study, we aimed to investigate the relationship between left ventricular hypertrophy (LVH) in HD patients and atherosclerosis and vascular calcification measured by electron beam computed tomography (EBCT). METHODS: In a cohort of 118 HD patients (52 male, 66 female, mean age: 46+/-13 years), we measured biochemical parameters, including BUN, creatinine, albumin, haemoglobin, C-reactive protein and fibrinogen levels, and performed echocardiography, high-resolution B-mode carotid ultrasonography and EBCT in 85 of them. The degree of stenosis was measured at four different sites (communis, bulbus, interna and externa) in both carotid arteries. Carotid plaque scores were calculated by summing the degrees of stenosis measured at all locations. RESULTS: LVH was detected in 89 of the patients (75%). Plaque-positive patients had higher left ventricular mass index (LVMI) than plaque-negative patients (175+/-59 vs 143+/-46 g/m2, P = 0.003). LVMI was correlated with systolic blood pressure (r = 0.62, P<0.001), pulse pressure (r = 0.58, P<0.001), haemoglobin levels (r = - 0.25, P = 0.008), carotid plaque score (r = 0.32, P = 0.001) and coronary (CACS) and aortic wall calcification score (AWCS) (r = 0.34, P = 0.002 and r = 0.43, P<0.001, respectively). Multiple linear regression analysis (model r = 0.76) showed the independent factors related to LVMI to be systolic blood pressure, pulse pressure, CACS and presence of carotid plaques. CONCLUSION: Extra-coronary atherosclerosis and vascular calcification are associated with LVH in HD patients. Whether the treatment of atherosclerosis or vascular calcification may cause regression of or even prevent LVH in HD patients remains to be seen.

[Reduced coronary collateral vessel recruitment capacity in diabetes mellitus: an evidence for defective ischaemic tolerance]. / Diyabetes mellitus'ta azalmis koroner kollateral damar açilma kapasitesi: defektif iskemik tolerans için bir kanit.

OBJECTIVE: Collateral channel opening is one of the components of the ischemic tolerance developing during subsequent coronary balloon occlusions. The effect of diabetes mellitus (DM) on coronary collateral recruitment (CR) is still not known. We therefore sought the effect of DM on CR in patients with stable angina pectoris (SAP) by using intracoronary pressure measurement technique. METHODS: Study material consisted of 44 patients (21 diabetic) with SAP. All of the patients had single vessel disease with more than 70% vessel narrowing and all of them underwent stent implantation to this vessel. After angiography, fiber-optic pressure monitoring guidewire was advanced distal to the stenosis to be dilated. Myocardial fractional flow reserve (FFRmyo) was determined under adenosine hyperemia by the ratio of simultaneously measured mean distal pressure to mean aortic pressure. During subsequent two 1 minute balloon occlusions, distal pressures were recorded as coronary wedge pressure (CWP). Collateral flow index was determined by the ratio of simultaneously measured CWP to mean aortic pressure. Percentage of the improvement in the coronary flow index (CFI) (first to second occlusion) between two occlusions was determined for each patient. RESULTS: There was no difference between two groups in terms of pre-intervention FFRmyo (0.54 +/- 0.12 in DM group and 0.50 +/- 0.11 in non-DM group). The baseline CFI was significantly higher in non-DM group (0.26 +/- 0.09 versus 0.17 +/- 0.08, p<0.03). Beyond this finding, mean CFI increased by 17% (from 0.17 +/- 0.08 to 0.20 +/- 0.09) in DM group and by 30% (from 0.26 +/- 0.09 to 0.34 +/- 0.10) in non- DM group. There was statistically significant difference between these two groups in terms of improvement in CFI during subsequent balloon occlusions (p<0.01). CONCLUSION: In addition to poor collateral vessels seen in patients with DM, CR is also impaired. This finding suggests that DM abolishes ischemic tolerance in terms of CR as well.

Effect of preinfarction angina pectoris on microcirculation in patients with reperfused acute myocardial infarction.

UNLABELLED: Preinfarction angina pectoris has been suggested in some studies to have a beneficial effect on left ventricular function after acute myocardial infarction (AMI). The precise mechanisms of this protection have not been fully elucidated. The effect of preinfarction angina on myocardial tissue perfusion also needs to be clarified. In this study, we investigated the influence of preinfarction angina on microvasculatory damage by using ST-segment resolution and pressure-derived collateral flow index (CFIp) as a marker of microcirculatory perfusion. METHODS: We studied 41 patients with a first AMI in whom thrombolysis in myocardial infarction (TIMI) grade 3 flow in the infarct-related artery was established by thrombolytic therapy. The percent resolution of ST-segment deviation (deltasigma ST) after thrombolysis was determined. All of the patients had TIMI grade 3 flow in IRA at the coronary angiography, which was done a mean of 4 days after AMI. Intracoronary pressure measurements and stent implantation to the IRA were performed. After angiography, CFIp was calculated as the ratio of simultaneously measured coronary wedge pressure-central venous pressure (Pv) to mean aortic pressure-Pv. RESULTS: Patients with preinfarction angina pectoris had greater percent deltasigma ST than those without PA (67 +/- 18% vs. 44 +/- 24%, p = 0.03). The mean of the coronary wedge pressure (16.4 +/- 7.4 compared with 23.2 +/- 9.4, P < 0.03) and the pressure-derived collateral flow index (0.15 +/- 0.10 compared with 0.22 +/- 0.08, P < 0.03) were significantly lower in patients with preinfarction angina compared to those without. CONCLUSION: Preinfarction angina is associated with a greater degree of ST-segment resolution and lower CFI-p in patients with TIMI-3 reflow after thrombolysis. These findings suggest that a protective effect of preinfarction angina against reperfusion injury may result in greater ST resolution and lower CFIp after AMI.

Carotid atherosclerosis is a predictor of coronary calcification in chronic haemodialysis patients.

BACKGROUND: Coronary artery calcification scores (CACS) calculated by electron beam computed tomography (EBCT) have been correlated with atherosclerotic burden in the non-uraemic population. However, the validity of this test in chronic haemodialysis patients (HD) is currently uncertain. In the present cross-sectional study, associations between carotid atherosclerosis and coronary calcification in HD patients are investigated. METHODS: We studied 79 chronic HD patients (39 male, 40 female; mean age, 45+/-12 years). The mean time on HD was 68+/-54 months (range, 6-187 months). In these patients, we measured serum calcium, phosphorus, total cholesterol, cholesterol subgroups and iPTH levels. EBCT, echocardiography, and high-resolution B-mode carotid Doppler ultrasonography were also performed. RESULTS: Plaque-positive HD patients had significantly higher CACS than plaque-negative patients (851+/-199 vs 428+/-185, mean+/-SE, P = 0.006). Coronary calcification scores were correlated with serum phosphorus (r = 0.37; P = 0.001). Only 8 of the 24 HD patients without coronary calcification had carotid plaques (33%), whereas 34 of the 53 patients with coronary calcification had carotid plaques (64%) (P = 0.015). Carotid plaque scores were correlated with CACS (r = 0.40; P = 0.001). A stepwise linear regression (model r = 0.72; P<0.001) revealed that CACS (log-transformed data of CACS) was associated with age (P<0.001), time on dialysis (P = 0.004), serum phosphorus level (P = 0.016) and carotid plaque scores (P = 0.037). CONCLUSIONS: Atherosclerosis is independently associated with coronary artery calcification and with hyperphosphataemia in chronic HD patients. CACS appeared to be predictive of both coronary atherosclerosis and carotid atherosclerosis.

Gene polymorphisms of endothelial nitric oxide synthase enzyme associated with pulmonary hypertension in patients with COPD.

In this cross-sectional controlled study, we aimed to investigate the role of polymorphisms of the angiotensin-converting enzyme (ACE) and endothelial nitric oxide synthase (eNOS) genes on pulmonary hypertension (PH) in patients with chronic obstructive pulmonary disease (COPD). Forty-two (41 male, 1 female, mean age: 62 +/- 7 years) COPD patients and 40 (all male, mean age: 60 +/- 8 years) healthy controls were included. Respiratory function tests, arterial blood gases, and echocardiographic examinations were performed. ACE and eNOS genotypes were determined using PCR. The ACE and eNOS genotype distribution was not significantly different between COPD patients and controls. On comparing pulmonary artery pressures in different eNOS genotypes, the mean pulmonary artery pressure (Ppa) in patients with the BB genotype was significantly higher than in patients with the nonBB genotypes (41.3 +/- 17.7 mmHg vs. 27.3 +/- 11.2 mmHg, P = 0.02). However, there was no difference in ACE genotype distributions between COPD patients with and without pulmonary hypertension. In stepwise linear regression analysis for predicting pulmonary artery pressure, PaO2 and polymorphism of eNOS gene were found to be independent variables. In conclusion, BB-type polymorphism of the eNOS gene has been associated with PH in addition to hypoxemia. However, ACE gene polymorphism was not found to be associated with PH.

Relationship between collateral blood flow and microvascular perfusion after reperfused acute myocardial infarction.

During acute occlusion of an epicardial vessel collaterals preserve the microvascular perfusion and limit the extent of myocardial damage. Pressure-derived collateral flow index (CFIp) assessed by intracoronary pressure measurement allow us to quantify collateral vessel development. The angiographic myocardial blush (MB) scores, based on the contrast dye density and washout in the infarcted myocardium, provide important information about microvascular perfusion after acute myocardial infarction (AMI). In this study we assessed the microvascular perfusion with MB and studied the relation between CFIp in patients with AMI who treated with thrombolytic therapy and TIMI grade III flow restored in the infarct related artery (IRA). Forty-one patients with AMI who were treated with thrombolytic therapy and underwent stent implantation (mean of 3 days after AMI) to the IRA were included in this study. After angiography, CFIp was calculated as the ratio of simultaneously measured coronary wedge pressure--central venous pressure (Pv) to mean aortic pressure--Pv. Myocardial blush was graded densitometrically based on visual assessment of the relative contrast opacification of the myocardial territory subtended by the infarct vessel. There was a statistically significant correlation between CFIp and post-stent myocardial blush grades (P < 0.01, r = 0.70). There was a significant difference in mean CFIp among myocardial blush grades implying that higher CFIp is associated with better MB (0.39 +/- 0.11 in grade 3, 0.32 +/- 0.10 in grade 2, 0.24 +/- 0.09 in grade 1, and 0.16 +/- 0.08 in grade 0, P < 0.01). Well developed collaterals can limit microvascular damage by preserving microvascular perfusion. A higher pressure-derived collateral flow index is associated with better tissue level perfusion as evidenced by the higher myocardial blush score.