Inflammatory mediators in chronic heart failure in North India.

INTRODUCTION: Recent evidence shows that pro-inflammatory cytokines may be important in the assessment of severity and prognosis in congestive heart failure (CHF). In the present study, we examine the association of cytokines with causes, grade and prognosis of CHF patients. SUBJECTS AND METHODS: Of 127 patients with CHF, 11 were excluded and the remaining 116 patients with different aetiologies of CHF, and 250 age- and sex-matched control subjects, were evaluated in this case study. Severity of disease based on the New York Heart Association (NYHA) standards, fell within functional classes II to IV. The diagnosis of HF was based on clinical manifestations as well as on echocardiographic heart enlargement. Cytokines were measured by chemiluminescence. Causes of death were assessed based on death certificates. Multivariate logistic regression analysis was used to determine the risk factors of heart failure. RESULTS: Echocardiographic ejection fraction was 39.1 +/- 8.2% (mean +/- SD) in the study group indicating class II-IV heart failure. Laboratory data showed increase in biomarkers of oxidative stress, among HF patients compared to healthy subjects. Pro-inflammatory cytokines; IL-6 and TNF-alpha were significantly higher among HF patients compared to healthy subjects. TNF-alpha and IL-6, showed significant increase among patients with CHF due to ischaemic heart disease and cardiomyopathy compared to levels among CHF patients with valvular heart disease and hypertensive heart diseases. The levels of the cytokines were significantly higher among patients with class III and IV heart failure and those who died, compared to patients with class II heart failure. Multivariate logistic regression analysis revealed that CAD, cardiomyopathy, and IL-6 were strongly associated--and low ejection fraction and TNF-alpha--weakly associated with HF. Of 116 patients, 20 (17.2%) died during a follow-up of two years, and the deaths were mainly among NYHA class III and IV patients in whom the cause of CHF was CAD (10.9%) and cardiomyopathy (6.9%) which had greater levels of cytokines. CONCLUSIONS: The findings indicated that pro-inflammatory cytokines may be important indicators of causes, severity of CHF and prognosis among these patients.

Intravascular ultrasound-guided percutaneous coronary interventions with minimum contrast volume for prevention of the radiocontrast-induced nephropathy: report of two cases.

Radiocontrast-induced nephropathy (CIN) is one of the most serious complications of percutaneous coronary interventions (PCI). The prevention of PCI-related CIN for chronic kidney disease (CKD) patients has not been established yet. The intravascular ultrasound (IVUS) is commonly used as an imaging device during PCI. We performed IVUS-guided PCI while only using fluoroscopic imaging and without administering any routine contrast dye injection during the procedures. All patients underwent a baseline coronary angiography prior to the elective PCI. During the PCI, all the following procedures were done with X-ray fluoroscopic imaging without or with a minimized contrast dye injection: the engagement of the guiding catheter, insertion of the coronary guidewire, insertion of the IVUS catheter, the stent deployment and the post-dilatation. The diameter and the length of the balloon and the stent were determined according to the pre-procedural IVUS findings, and the end point of the stent dilatation was also judged according to the acquired minimal cross-sectional area of the stent. Here we report our findings from two cases representative of IVUS-guided minimum contrast PCI in which the volumes of contrast dye during the procedure were 5 and 4 ml, respectively. No CIN occurred after either procedure. The IVUS-guided minimum contrast PCI could be a promising option for the prevention of CIN after PCI.

A simple method preventing tangling of the guidewires during percutaneous coronary intervention for bifurcation lesions.

The aim was to examine the efficacy of the simple technique that reduces tangling of the guidewires by utilizing wet gauze during percutaneous coronary intervention with multiple guidewires. We defined "Critical tangle of the guidewires" as occurring when it became impossible to insert balloon catheters into the bifurcation lesion due to tangling of the guidewires without withdrawing and reinserting one of the guidewires. We compared the rate of the critical tangle of the guidewires between the group taking no special tangle precaution ("NP Group"), and the group taking the tangle precaution with the wet gauze ("Gauze Group"). Eighty-four patients were enrolled in the study and randomly assigned to either NP Group (n = 43) or Gauze Group (n = 41). The kissing balloon technique success was 42/43 (97.7%) versus 40/41 (97.6%), in NP Group and Gauze Group, respectively. The rate of critical tangle of the guidewires was significantly lower in Gauze Group (27.9 vs. 7.3%, p = 0.014). The manipulation of several guidewires utilizing gauze method will be a useful technique for reducing tangle of the guidewires during the procedure of kissing balloon technique.

Potential difficulty for accurate categorization of drug-eluting stent thrombosis without coronary angiography: unignorable involvement of the cases with new onset acute myocardial infarction occurred in target vessels.

Very late stent thrombosis (VLST) is a major unresolved problem of drug-eluting stent (DES) implants. However, its actual incidence with respect to the distribution of DES-target vessel and accuracy of adjudicating stent thrombosis according to the ARC definition has not been yet adequately evaluated. We studied 720 patients who had completed over 1 year from elective DES implantation. In this cohort, we extracted patients who present acute coronary syndrome (ACS) (n = 3, 0.4%). The timing of ACS events was 17, 19, and 24 months after DES implantation. At the time of presentation, VLST was strongly suspected as the initial diagnosis, however, coronary angiography (CAG) confirmed the different culprit lesion from DES and clearly no thrombus within the DES. According to ARC definition, three probable stent thromboses in this cohort before CAG, however, no stent thrombosis was confirmed after the CAG. Thus, no stent thrombosis was confirmed among this study population. In the very late phase after DES implantation, new onset ACS is not at all extraordinary occurrence in the target vessels of previous DES implantation. However, stent thrombosis is often assumed without angiographic confirmation. The clinical possibility that non-stent thrombosis is incidentally diagnosed with stent thrombosis without angiographic confirmation should be considered within the current accepted definition of stent thrombosis.

Atrial fibrillation induced by applying acetylcholine to subadventitial layer of pulmonary vein in normal canine heart.

OBJECTIVES: We determined whether acetylcholine (Ach) application to the pulmonary vein (PV) wall could induce AF and clarified its mechanisms, and determined whether circumferential PV radiofrequency ablation (CPVA) could prevent Ach-induced AF in canine hearts. METHODS: Thirty seven beagle dogs were used for the study. Ach was injected into the subadventitial layer of the left superior PV (LSPV), at different distance from the LSPV-left atrium junction (LSPV-LA-J) to locate AF initiation. When AF was not induced by Ach alone, programmed electrical stimulation (S1-S2 method) was added to elicit AF. Atropine was injected at the same site of Ach injection to determine whether muscarine-receptor blockade suppressed AF, and CPVA at the LSPV-LA-J was performed using a newly devised basket electrode-catheter. RESULTS: AF was reproducibly induced by Ach injection in 19 of the 26 dogs (73%). S1-S2 method after Ach initiated AF in 5 of the remaining 7 dogs. Ach into the subadventitial layer of the LSPV, especially the distal portion, could elicit AF, which was preceded by pause (sinus arrest) ≥ 2.0 sec (37%) (pause-AF group), sinus bradycardia (32%) (brady-AF group) and sinus tachycardia (32%) (tachy-AF group). The time from Ach injection to AF initiation and AF duration were not significantly different between pause-AF, brady-AF and tachy-AF groups. AF was not initiated by injecting Ach after atropine pretreatment. To eliminate AF, 1-6 (average 4.1 ﾂｱ 1.2) CPVAs at the LSPV-LA-J were required. CONCLUSIONS: Our observations suggest that local Ach application can initiate AF in PVs, preceded by a variety of modes such as pause, bradycardia or tachycardia, and an increase in vagal tone at the LSPV plays a critical role in eliciting AF in structurally normal heart.

Possible mechanism of preventive effects of coffee intake on the formation of arterial occlusive thrombosis.

BACKGROUND: Prevalence and incidence of arterial occlusive thrombosis are influenced by life-style. Coffee consumption was shown with a lower incidence of myocardial infarction by Framingham Study. Yet, the mechanism is to be elucidated. METHODS: We examined the effects of coffee intake on the progression of occlusive thrombus formation in mouse cremasteric arteries. After 7 days of free intake of pure water, coffee containing water (5 mg/ml), or caffeine containing water (0.1 mg/ml), endothelial cell function was locally damaged by FeCl3. Circulating platelet and leukocytes were rendered fluorescently by rhodamine 6G. Process of occlusive thrombus growth was continuously visualized by 3-D imaging system equipped with ultra-fast confocal microscopy, and time to vascular occlusion was measured in each mouse. RESULTS: Platelet accumulation started immediately after FeCl3 exposure in all tested groups. However, arterial occlusion time in taking coffee containing water was significantly longer than those taking pure water. (46.0 ± 17.4 min (n = 5) vs. 12.3 ± 2.6 min (n = 31), p < 0.05) Arterial occlusion time in mice taking caffeine (13.8 ± 5.9 min (n = 4)) was not different from those taking pure water. CONCLUSION: Coffee, but not caffeine intake, may have preventive effect on arterial occlusive thrombus formation initiated by functional injury of arterial endothelium.

Analysis of right radial artery for transradial catheterization by quantitative angiography--anatomical consideration of optimal radial puncture point.

OBJECTIVES: To determine the optimal radial puncture point, we analyzed the anatomy and luminal diameter of the right radial artery (RA) by quantitative angiography. BACKGROUND: Difficulty of radial puncture has impeded the establishment of the transradial approach as the standard procedure for cardiac catheterization. METHODS: Antegrade angiography was performed from the right brachial artery in 135 patients who underwent coronary angiography. Presence and location of a bifurcation in the area of the RA puncture were analyzed. Furthermore, inner luminal diameter of the RA was quantitatively measured. We used the line between the styloid process and the ulnar styloid process (R-U line) as an anatomical reference point. RESULTS: Radial arterial bifurcation with a superficial palmar branch was angiographically observed in 66 patients (48.9%). The inner luminal diameter was significantly larger at the proximal point to the point of bifurcation. The bifurcation level was located at a median of -3.33 mm (interquartile range: -5.60 to 4.69 mm) below the R-U line. Radial puncture at 10 mm proximal to the R-U line could avoid bifurcation in 91.9% of all cases. Mean radial, ulnar and brachial arterial inner diameters were 2.94 +/- 0.52 mm, 2.51 +/- 0.49 mm and 4.53 +/- 0.62 mm. The RA size within 10-60 mm above the R-U line was nearly invariable throughout the range. CONCLUSION The radial puncture level should be proximal to the radial bifurcation because of its lumen size. The ideal puncture point was found to be at least 10 mm proximal to the R-U line.

Angiographic evaluation of right upper-limb arterial anomalies: implications for transradial coronary interventions.

OBJECTIVES: Upper-limb arterial anomalies are sometimes encountered during transradial coronary procedures. These anomalies may contribute to procedural failure or to vascular complications, and are a major reason why many operators tend to avoid transradial procedures. We investigated the frequency of right upperlimb arterial anomalies using antegrade arteriography in patients undergoing transbrachial coronary angiography or intervention, and discuss the potential impact of these anomalies on the transradial procedure. METHODS: We prospectively studied 163 consecutive patients who underwent right transbrachial coronary angiography or intervention for the first time during the period from May 2007 to December 2007. Following the transbrachial procedure, we performed antegrade transbrachial arteriography of right upper-limb arteries in these patients and investigated the frequency and anatomy of arterial anomalies. RESULTS: A total of 40 upper-limb arterial anomalies were observed in 38 patients (23.3%). These included 8 abnormal origins (4.9%), 2 radio-ulnar loops (1.2%), 25 tortuosities (15.3%), 4 stenoses (2.5%) and 1 loop (0.6%). In patients with congenital lesions (8 patients; 4.9%), abnormal origin of the radial artery was the most common anomaly encountered, and in the acquired group (25 patients; 15.3%), tortuosity was the most common abnormality. CONCLUSION: Even with a 23.3% incidence of right upper-limb arterial abnormalities, 98.8% of patients were acceptable for transradial coronary intervention except for 1.2% of radio-ulnar loops.

Important regulatory role of activated platelet-derived procoagulant activity in the propagation of thrombi formed under arterial blood flow conditions.

BACKGROUND: The functional links between the activation of platelets and the coagulation system have not been clarified. METHODS AND RESULTS: Immobilized collagen fibrils were perfused with human blood containing fluoresceinated platelets in the presence of various concentrations of thrombin inhibitor. Coagulant activity around platelet thrombi was detected using a FITC-conjugated antibody against the fibrin monomer complex (F-405). Intra-cytosolic calcium ion concentrations ([Ca(2+)](i)) in individual platelets and the volume of thrombi were detected with an ultrafast confocal laser microscope equipped with a piezo-motor control unit. The volume of platelet thrombi formed after 8 min of blood perfusion in the presence of 10, 25, 50, and 100 micromol/L argatroban was 7.69+/-0.46 microm(3), 6.61+/-1.96 microm(3), 3.63+/-1.54 microm(3), and 1.67+/-0.75 microm(3), respectively. There was a positive correlation between the volume of platelet thrombi and the amount of fibrin monomer complex produced around them. The [Ca(2+)](i) of the platelets forming the thrombi oscillated between a minimum of 92.0+/-57.4 nmol/L, 120.1+/-68.1 nmol/L, and a maximum of 217.6+/-131.5 nmol/L, 367.6+/-189.1 nmol/L, respectively, in the presence of 100 and 10 mumol/L argatroban. CONCLUSIONS: The results suggest a crucial role of coagulant activity in both the generation of fibrin and the growth of platelet thrombi.