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Chronic inflammation plays a pivotal role in the development of atherosclerosis, where the pro-inflammatory cytokine-induced expression of endothelial adhesion molecules and the recruitment of monocytes are the crucial events leading to its pathogenesis. Glossogyne tenuifolia ethanol extract (GTE) is shown to have potent anti-inflammatory and antioxidant activities. We evaluated the effects of GTE and its major components, luteolin (lut), luteolin-7-glucoside (lut-7-g), and oleanolic acid (OA) on TNF-α-induced expression of adhesion molecules in human umbilical vein endothelial cells (HUVECs). The results demonstrated that GTE, lut, and lut-7-g attenuated the expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in TNF-α-activated HUVECs, and inhibited the adhesion of monocytes to TNF-α-activated HUVECs. The TNF-α-induced mRNA expression of ICAM-1 and VCAM-1 was also suppressed, revealing their inhibitory effects at the transcriptional level. Furthermore, GTE, lut, and lut-7-g blocked the TNF-α-induced degradation of nuclear factor-kB inhibitor (IkB), an indicator of the activation of nuclear factor-kB (NF-kB). In summary, GTE and its bioactive components were effective in preventing the adhesion of monocytes to cytokine-activated endothelium by the inhibition of expression of adhesion molecules, which in turn is mediated through blocking the activation and nuclear translocation of NF-kB. The current results reveal the therapeutic potential of GTE in atherosclerosis.

Background Blunt cardiac trauma encompasses a wide range of clinical entities, including myocardial contusion, cardiac rupture, valve avulsion, pericardial injuries, arrhythmia, and even myocardial infarction. Acute myocardial infarction due to coronary artery dissection after blunt chest trauma is rare and may be life threatening. Differential diagnosis of acute myocardial infarction from cardiac contusion at this setting is not easy. Case presentation Here we demonstrated a case of blunt chest trauma, with computed tomography detected myocardium enhancement defect early at emergency department. Under the impression of acute myocardial infarction, emergent coronary angiography revealed left anterior descending artery occlusion. Revascularization was performed and coronary artery dissection was found after thrombus aspiration. Finally, the patient survived after coronary stenting. Conclusion Perfusion defects of myocardium enhancement on CT after blunt chest trauma can be very helpful to suggest myocardial infarction and facilitate the decision making of emergent procedure. This valuable sign should not be missed during the initial interpretation.

Background Ischemic mitral regurgitation (IMR) is common in ischemic heart disease and results in poor prognosis. However, the exact mechanism of IMR has not been fully elucidated. Hypothesis Quantitation of the mitral tetrahedron using three-dimentianl (3D) echocardiography is capable of evaluating the geometric determinants and mechanisms of IMR. Methods Forty patients with a history of ST-elevation myocardial infarction at least 6 months earlier were studied. Parameters of mitral deformation and global left ventricular (LV) function and shape were evaluated by 2-dimensional echocardiography. The effective regurgitant orifice (ERO) of IMR was obtained by the quantitative continuous-wave Doppler technique. Three-dimensional (3D) echocardiography was applied to assess the mitral tetrahedron. Results Mitral valvular tenting area (P

To evaluate the efficacy and safety of valsartan in Taiwanese patients with essential hypertension.This 12-week multi-center, open-label, observational, post-marketing surveillance study enrolled 2046 hypertensive patients who were prescribed valsartan 80 or 160 mg as monotherapy or in combination with other antihypertensives based on clinical judgment. The primary endpoint was the incidence rate of dizziness with valsartan 160 mg monotherapy or combination therapy at Week 4. Secondary endpoints included the blood-pressure-lowering efficacy and the overall safety and tolerability of valsartan at Weeks 4 and 12.The monotherapy and combination groups had comparable baseline characteristics. At Week 4, monotherapy was found non-inferior to combination for incidence rate of dizziness (monotherapy, 9.25%; combination, 10%; difference in incidence of dizziness, 0.75%; 95% CI - 0.61% to 2.12%; non-inferiority margin, -1.33%;WaldTest approach). Greater blood pressure (BP) reduction was noted atWeek 12 than atWeek 4.The antihypertensive effect was greater with combination therapy and the 160-mg dose. BP control (systolic140 mmHg or diastolic90 mmHg) was achieved in 80-90% patients.Valsartan was well tolerated; most commonly reported adverse events included dizziness, headache, constipation and cough.Valsartan is an effective treatment option for essential hypertension in Taiwanese patients.

Background We compared the haemodynamic and metabolic effects of acetyl-L-carnitine (one of the carnitine derivatives) and of oxfenicine (a carnitine palmitoyltransferase-1 inhibitor) in streptozotocin-induced diabetes in male Wistar rats. Materials and methods Diabetes was induced by a single tail vein injection of 55 mg kg )1 streptozotocin. The diabetic animals daily treated with either acetyl-L-carnitine (150 mg kg )1 in drinking water) or oxfenicine (150 mg kg )1 by oral gavage) for 8 weeks,were compared with the untreated age-matched diabetic controls. Arterial wave reflection was derived using the impulse response function of the filtered aortic input impedance spectra. Thiobarbituric acid reactive substances (TBARS) measurement was used to estimate malondialdehyde (MDA) content. Results Oxfenicine, but not acetyl-L-carnitine, increased total peripheral resistance in diabetes, which paralleled its elevation in plasma levels of free fatty acids. By contrast, acetyl-L-carnitine, but not oxfenicine, resulted in a significant increase in wave transit time and a decrease in wave reflection factor, suggesting that acetyl-L-carnitine may attenuate the diabetes-induced deterioration in systolic loading condition for the left ventricle. This was in parallel with its lowering of MDA ⁄TBARS content in plasma and aortic walls in diabetes. Acetyl-L-carnitine therapy also prevented the diabetes-related cardiac hypertrophy, as evidenced by the reduction in ratio of the left ventricular weight to body weight. Conclusion Acetyl-L-carnitine, but not oxfenicine, attenuates aortic stiffening and cardiac hypertrophy, possibly through its decrease of lipid oxidation-derived MDA ⁄TBARS in the rats with insulin deficiency.

Background and purpose: Our team previously demonstrated that diabetes induces a deterioration in vascular dynamics, in parallel with the enhanced formation of advanced glycation end products. The aim of this study was to determine whether prevention of the arterial stiffening by pyridoxamine in diabetes is associated with inhibition of the pathogenic glycation on aortic collagen. Experimental approach: Diabetes was induced in rats by a single tail vein injection with 55 mg·kg -1 steptozotocin (STZ). After induction of hyperglycaemia, animals were treated for 8 weeks with pyridoxamine (1 g·L -1 in drinking water) and compared with the age-matched untreated diabetic controls. Pulse wave reflection along the vasculature was derived using the impulse response function of the filtered aortic input impedance spectra. Keyresults: Treatment of this experimental diabetes with pyridoxamine resulted in a significant increase in wave transit time and a decrease in wave reflection factor, indicating that pyridoxamine attenuates the diabetes-induced augmentation in systolic load of the left ventricle coupled to its arterial system. Meanwhile, pyridoxamine therapy ameliorated the diabetes-related cardiac hypertrophy, as evidenced by the reduction in ratio of the left ventricular weight to body weight. Glycation-derived modification of aortic collagen was also found to be attenuated by administration of pyridoxamine to the STZ-induced diabetic rats. Conclusions and implications: Pyridoxamine imparts significant protection against the diabetes-induced deterioration in pulsatile arterial load imposed on the heart, at least partly through inhibition of the formation of advanced glycation end products and their accumulation on aortic collagen of the STZ-treated rats. British Journal of Pharmacology (2009) 157, 1419–1426; doi:10.1111/j.1476-5381.2009.00309.x

Oleic acid (OA) affects assembly of gap junctions in neonatal cardiomyocytes. Adherens junction (AJ) regulates the stability of gap junction integrity; however, the effect of OA on AJ remains largely unexplored. The distribution of N-cadherin and catenins at cell-cell junction was decreased by OA. OA induced activation of protein kinase C(PKC)-alpha and -epsilon and Src family kinase, and all three kinases were involved in the oleic acid-induced disassembly of the adherens junction, since it was blocked by pretreatment with Gö6976 (a PKCalpha inhibitor), epsilonV1-2 (a PKCepsilon inhibitor), or PP2 (a Src family kinase inhibitor). Src family kinase appeared to be the downstream of PKC-alpha and -epsilon, as blockade of either PKC-alpha or -epsilon activity prevented the OA-induced activation of Src family kinase. Immunoprecipitation analyses showed that OA activated Fyn and Fer. OA promoted the association of p120 catenin/beta-catenin with Fyn and Fer and caused increased tyrosine phosphorylation of p120 catenin and beta-catenin, resulting in decreased binding of the former to N-cadherin and of the latter to alpha-catenin. Pretreatment with PP2 abrogated this OA-induced tyrosine phosphorylation of p120 catenin and beta-catenin and restored the association of N-cadherin with p120 catenin and that of beta-catenin with alpha-catenin. In conclusion, these results show that OA activates the PKC-Fyn signaling pathway, leading to the disassembly of the AJ. Therefore, inhibitors of PKC-alpha/-epsilon and Src family kinase are potential candidates as cardioprotection agents against OA-induced heart injury during ischemia-reperfusion.

Background Diastolic heart failure (DHF) refers to an abnormality of diastolic distensibility, filling or relaxation of the left ventricle. The genetic study of DHF is scarce in the literature. The association of renin-angiotensin system (RAS) and DHF are well known. We hypothesized that RAS genes might be the susceptible genes for DHF and conducted a case-control study to prove the hypothesis. Materials and methods A total of 1452 consecutive patients were analysed and 148 patients with a diagnosis of DHF confirmed by echocardiography were recruited. We had two control populations. The first controls consisted of 286 normal subjects while the second were 148 matched controls selected on a 1-to-1 basis by age, sex, hypertension, diabetes and medication use. The angiotensin-converting enzyme (ACE) gene insertion/deletion polymorphism; multilocus polymorphisms of the angiotensinogen gene; and the A1166C polymorphisms of the angiotensin II type I receptor (AT1R) gene were genotyped. Results In a single-locus analysis, the odds ratios (ORs) for DHF were significant with the ACE DD genotype and the AT1R 1166 CC plus AC genotype. In addition, the concomitant presence of ACE DD and AT1R 1166 CC/AC genotypes synergistically increased the predisposition to DHF. Conclusions Genetic variants in the RAS genes may determine an individual's risk to develop DHF. There is also a synergistic gene-gene interaction between the RAS genes in the development of DHF.

Background Our team previously demonstrated arterial stiffening and cardiac hypertrophy in type 2 diabetic rats at 8 but not 4 weeks after being administered streptozotocin (STZ) and nicotinamide (NA). The present study focused on investigating the effects of type 2 diabetes on cardiac autonomic nerve function in the STZ- and NA-treated animals, using modern spectral estimation technique. Design An autoregressive process was performed to each detrended signal of heart rate and systolic blood pressure measured in the 4- and 8-week STZ-NA rats with anaesthesia. The power of low-frequency and high-frequency oscillations was automatically quantified with each spectral peak by computing the residuals. The closed-loop baroreflex gain was estimated using the square root of the ratio between heart rate and systolic blood pressure powers in the low-frequency band. Results Compared with the age-matched controls, both the 4- and 8-week STZ-NA diabetic rats had significantly decreased low-frequency oscillations of heart rate but not systolic blood pressure variability, showing a decline in baroreflex gain (0·451 ± 0·060 and 0·484 ± 0·056 vs. 1·196 ± 0·064 ms mmHg−1, P

To study the association of renin gene polymorphism with essential hypertension in the Chinese population, 86 hypertensive and 107 normotensive subjects were enrolled from an epidemiologic survey. Leukocyte DNA was extracted and digested with Hind III and Bgl I restriction enzymes. Southern hybridization was done with digoxigenin-incorporated renin gene probes generated by polymerase chain reaction. The restriction fragments were detected by anti-digoxigenin antibody and enzyme methods. Two Hind III polymorphysms of the renin gene (8.7 kb and 6.2 kb) were identified. The allele frequences were 129(75%) and 43(25%), respectively, in hypertensives; they were 139(65%) and 75(35%), respectively, in normotensives (chi2 = 4.074, p = 0.044). The genotypes of 8.7/8.7,8.7/6.2 and 6.2/6.2 were significantly different between hypertensives and normotensives, being 45(52%), 39(45%), 2(3%) and 48(45%), 43(40%), and 16(15%), respectively (chi2 = 9.002, p = 0.11). The Bgl I polymorphism did not show a difference between hypertensives and normotensives. Thus, we conclude that the renin gene Hind III polymorphysm is associated with hypertension in this Chinese population.

Background/Purpose Drug eluting stents (DES) have been shown to reduce in-stent restenosis rate and target vessel revascularization in large clinical trials. However, the safety and efficacy of DES use in the Taiwanese population has not been reported. We designed this trial to analyze the clinical results in patients using DES in a single tertiary center. Methods We retrospectively analyzed the clinical data of all patients treated at National Taiwan University Hospital, Taipei, Taiwan, with sirolimus- or paclitaxel-eluting stents between September 2003 and January 2005. Results A total of 585 patients (466 men, 119 women; mean age, 64.5 ± 11.2 years) were enrolled. Meanwhile, 205 sirolimus- and 717 paclitaxel-eluting stents were implanted, with a mean of 1.6 stents per patient. Half (50.2%) of the stents were placed in the left anterior descending artery. Among the enrolled patients, 41.8% had diabetes mellitus, 25% had a diagnosis of acute coronary syndrome, and 10.7% was treated with primary percutaneous coronary intervention for ST-segment elevation myocardial infarction. Overall 8-month target vessel revascularization, major adverse cardiac event rate, and cardiac death rate were 8.8%, 9.7% and 2.5%, respectively. There was no difference in clinical events between sirolimus- and paclitaxel-eluting stents. The overall subacute stent thrombosis rate was 1.36%, significantly lower than that in patients who presented with acute coronary syndrome (4%). Conclusion The use of DES in the Taiwanese population yielded comparable results as those in large clinical trials. Subacute stent thrombosis rate was higher in acute coronary syndrome. The safety of DES in these situations should be further clarified.

Background: The clinical predictors of inflammation in atherosclerosis remain controversial. The objective of this study was to compare the associations of metabolic factors vs. infectious burden (IB) with inflammation, the severity of coronary atherosclerosis, and major adverse cardiovascular events (MACEs). Design, Setting, and Patients: Coronary angiography with Gensini score was applied to assess the severity of coronary atherosclerosis in 568 patients with coronary artery disease. Metabolic syndrome (MS) score (0–5) was defined according to the modified criteria of National Cholesterol Education Program Adult Treatment Panel III. IB score (0–7) was defined as the number of seropositivities to several agents. Results: IB score was not associated with plasma C-reactive protein (CRP) concentration, Gensini score, or the risk of MACE. In contrast, MS score significantly correlated with both plasma CRP concentration and Gensini score (P < 0.001 for both). MS score and plasma CRP concentration were also significantly associated with the risk of MACE (hazard ratios 1.51, P < 0.001; and 1.90, P = 0.002, respectively). Conclusion: Compared with IB, metabolic abnormalities have a more prominent association with the degree of inflammation, the severity of coronary atherosclerosis, and the risk of MACE in patients with coronary artery disease.

Background/purposeElevation of C-reactive protein (CRP) level is associated with increased risk of cardiovascular events. The 1059 G > C polymorphism in exon 2 of the CRP gene has been shown to affect plasma concentration of CRP. We want to elucidate the effect of this polymorphism on the development of coronary artery disease (CAD) among the Chinese population in Taiwan.MethodsWe scrutinized 536 patients undergoing coronary angiography (365 patients with CAD and 171 controls with patent coronaries) and evaluated the association of CRP gene 1059 G > C polymorphism with CAD. Genotyping of the polymorphism was performed by polymerase chain reaction and MaeIII restriction enzyme digestion.ResultsThe CC genotype was associated with lower plasma CRP concentration (GG, 6.5 ± 5.8; GC, 3.3 ± 4.4; CC, 2.3 ± 3.1 mg/L; p = 0.02). Subjects with CAD or myocardial infarction (MI) had significantly higher plasma CRP concentration than that in controls (CAD vs. controls, 8.9 ± 18.9 vs. 3.3 ± 7.2 mg/L; p < 0.001), while patients with MI showed higher CRP when compared to those with chronic stable angina (13.5 ± 22.9 vs. 5.2 ± 14.1 mg/L; p < 0.001). However, this polymorphism was not associated with CAD in our population.ConclusionOur data suggest that human CRP gene 1059 G > C polymorphism is associated with plasma CRP concentration among Chinese in Taiwan receiving coronary angiography.

The formation of advanced glycation endproducts (AGEs) on collagen within the arterial wall may be responsible for the development of diabetic vascular injury. This study was to examine the role of aminoguanidine (AG), an inhibitor of AGEs formation, in the prevention of arterial stiffening and cardiac hypertrophy in streptozotocin (STZ) induced diabetes in rats. Diabetes was induced in animals by a single tail vein injection with 65 mg kg−1 STZ. After confirmation of the development of hyperglycemia (2 days later), rats were treated for 8 weeks with AG (daily peritoneal injections of 50 mg kg−1) and compared with the age-matched untreated diabetic controls. After exposure to AG, the STZ-diabetic rats showed no alterations in cardiac output, aortic pressure profiles, total peripheral resistance, and aortic characteristic impedance. By contrast, treatment of this experimental diabetes with AG resulted in a significant increase in wave transit time (τ), from 20.4±0.6 to 24.7±0.5 ms (P

In recent studies, aminoguanidine (AG), an inhibitor of advanced glycation endproducts, has been identified as a prominent agent that can prevent the age-related aortic stiffening and cardiac hypertrophy. The aim of this study was to determine whether AG had effects on the left ventricular (LV)-arterial coupling in aged Fisher 344 rats in terms of the ventricular and arterial chamber properties. Normotensive rats were treated from 18 to 24 months with AG (1 g l(-1) in drinking water) and compared with a control group. LV pressure and ascending aortic flow signals were recorded to construct the ventricular and arterial end-systolic pressure-stroke volume relationships to calculate LV end-systolic elastance (Ees) and effective arterial volume elastance (Ea), respectively. The optimal afterload (Qload) determined by the ratio of Ea to Ees was used to measure the efficiency of mechanical energy transferred from the left ventricle to the arterial system. In comparison with the 6-month-old rats, the 24-month-old animals had decreased Ees, at 567.4 +/- 26.7 vs 639.0 +/- 20.7 mmHg ml(-1), decreased Ea, at 411.5 +/- 18.6 vs 577.9 +/- 15.7 mmHg ml(-1), and decreased Q(load), at 0.9428 +/- 0.0024 vs 0.9962 +/- 0.0014. Treatment with AG for 6 months did not significantly affect Ees; however, when normalized to LV weight (i.e., Eesn = Ees/LV weight), Eesn showed a significant rise of 22.8%, suggesting that AG may retard the aging process on the intrinsic contractility of the left ventricle. On the other hand, the decrease in Ea in aging rats was prevented by AG, as reflected in the increase of 19.7% in this variable (P < 0.05). The 24-month-old treated rats also exhibited a significant rise of 21.6% in Ea/Ees, causing an increase of 5.2% in Qload (P < 0.05). We conclude that in healthy older Fisher 344 rats without diabetes, long-term treatment with AG may improve both the arterial and ventricular function and optimize the matching condition for the left ventricular-arterial coupling.

Although some single polymorphism analyses of the angiotensinogen (AGT) gene have been found to be associated with hypertension, the results are still inconsistent. The objectives of this study are to evaluate the association of the genotype and haplotype distributions of three single-nucleotide polymorphisms (SNPs) (G-217A, A-6G, and M235T) in the AGT gene with hypertension. In a sample of 461 hypertensive and 327 normotensive patients in Taiwan, we found that -217AA and -6GG homozygotes conferred independently an increased risk to hypertension (P = 0.008 and P = 0.037, respectively), as illustrated by their significant associations with hypertension in both single SNP and pair-wise SNPs analyses. Meanwhile, a very weak linkage disequilibrium was found between the G-217A and the A-6G polymorphisms in terms of r2 (0.05). On the basis of likelihood ratio test, only the set of haplotypes that constituted the A-6G and the M235T polymorphisms was associated with hypertension (chi2 = 20.91, P = 0.0008), which was mainly due to the increased frequency of the recombinant haplotypes (-6A identical with 235M and -6G identical with 235T), and a pathophysiological role in the predisposition to hypertension was hence indicated. In functional assays, the promoter activities of the haplotypes -217A identical with -6A and -217G identical with -6G were significantly higher than the most common haplotype -217G identical with -6A. These results highlight the necessity of a thorough analysis of all reported variants of a candidate gene in the elucidation of genetic susceptibility to a complex disease like hypertension, even when the variants are in the same haplotype block.

OBJECTIVE: Polymorphisms of the angiotensinogen (AGT) gene, especially in the promoter region, are in linkage concordance and are associated with hypertension. In this study, we examined the role of AGT promoter polymorphisms, including G-217A, A-6G and M235T variants, and their promoter function in essential hypertension in Taiwanese populations. DESIGN: An association study was conducted to assess the genotype distribution between hypertensive patients and normotensive subjects. We also used a transient transfection assay to examine basal transcriptional activity of G-217A and A-6G variants in a mammalian cell system. METHODS: Hypertensive subjects (390) and normotensive controls (388) of Taiwanese ethnicity were genotyped for the AGT G-217A, A-6G and M235T variants. Promoter activity was studied by cloning the promoter region (-614 to +41 bp) of AGT into the pSEAP2-Basic reporter vector and performing a transient transfection assay in HuH7 and HepG2 cells. RESULTS: The G-217A variant of the AGT gene was significantly associated with hypertension (P = 0.0047), but the A-6G and M235T polymorphisms were not (P = 0.17 and P = 0.33, respectively). Furthermore, the recessive model of homozygous genotype (-217AA) conferred a high risk for hypertension (odds ratio 3.64) in this population. The -217A variant expressed higher transcriptional activity than -217G in vitro. CONCLUSIONS: Our study showed a significant association between the -217A variant of the AGT gene and hypertension. This variant plays a functional role in basal transcription of AGT, and may confer a risk for hypertension in Taiwanese populations.

We determined the effects of long-term treatment with aminoguanidine (AG), an inhibitor of advanced glycation end products, on the mechanical properties of the arterial system in aged Fisher 344 rats, using the aortic impedance analysis. Normotensive rats were treated from 18 to 24 months with AG (1 g/l−1 in drinking water) and compared with a control group. Pulsatile aortic pressure and flow signals were measured and then subjected to Fourier transformation for the analysis of aortic input impedance. Wave transit time was determined using the impulse response function of the filtered aortic input impedance spectra. With no alteration in body weight, rats treated with AG had decreased heart weight compared with the aged untreated controls. AG did not affect arterial blood pressure; however, the age-related increase in total peripheral resistance was prevented by AG. AG retarded the age-related decline in aortic distensibility, as evidenced by a reduction of 25.2% in aortic characteristic impedance and an increase of 28.1% in wave transit time. Meanwhile, the increase in wave reflection factor in aging rats was reduced by 32.3% by AG. Both the increased wave transit time and the decreased wave reflection factor suggest that AG may prevent the age-related augmentation in systolic loading condition for the left ventricle coupled to the arterial system. We conclude that long-term treatment with AG may impart significant protection against aortic stiffening and cardiac hypertrophy in aged Fisher 344 rats. British Journal of Pharmacology (2003) 140, 107–114. doi:10.1038/sj.bjp.0705410

We determined the effects of diabetes and gender on the physical properties of the vasculature in streptozotocin (STZ)-treated rats based on the aortic input impedance analysis. Rats given STZ 65 mg/kg i.v. were compared with untreated age-matched controls. Pulsatile aortic pressure and flow signals were measured and were then subjected to Fourier transformation for the analysis of aortic input impedance. Wave transit time was determined using the impulse response function of the filtered aortic input impedance spectra. Male but not female diabetic rats exhibited an increase in cardiac output in the absence of any significant changes in arterial blood pressure, resulting in a decline in total peripheral resistance. However, in each gender group, diabetes contributed to an increase in wave reflection factor, from 0.47 ± 0.04 to 0.84 ± 0.03 in males and from 0.46 ± 0.03 to 0.81 ± 0.03 in females. Diabetic rats had reduced wave transit time, at 18.82 ± 0.60 vs 21.34 ± 0.51 msec in males and at 19.63 ± 0.37 vs 22.74 ± 0.57 msec in females. Changes in wave transit time and reflection factor indicate that diabetes can modify the timing and magnitude of the wave reflection in the rat arterial system. Meanwhile, diabetes produced a fall in aortic characteristic impedance from 0.023 ± 0.002 to 0.009 ± 0.001 mmHg/min/kg/ml in males and from 0.028 ± 0.002 to 0.014 ± 0.001 mmHg/min/kg/ml in females. With unaltered aortic pressure, both the diminished aortic characteristic impedance and wave transit time suggest that the muscle inactivation in diabetes may occur in aortas and large arteries and may cause a detriment to the aortic distensibility in rats with either sex. We conclude that only rats with male gender diabetes produce a detriment to the physical properties of the resistance arterioles. In spite of male or female gender, diabetes decreases the aortic distensibility and impairs the wave reflection phenomenon in the rat arterial system.

Objective To investigate both the use of immediate or elective double-balloon pericardiotomy (DBP) in patients with a large amount of malignancy-related pericardial effusion, and the prognosis of this subgroup. Design Observational study after DBP intervention. Setting Tertiary referral center. Patients and interventions Fifty patients with malignancy, mainly lung and breast cancer, who were admitted to our critical care unit with a large amount of pericardial effusion. All received echocardiographic-guided pericardiocentesis. Group 1 consisted of 12 patients (24%) who received immediate DBP, and group 2 consisted of 38 patients (76%) who received delayed DBP 2.5 ± 1.7 days later (mean ± SD) after emergency pericardiocentesis with pigtail catheter drainage. Measurements After the procedure, and at 1 month, 3 months, and 6 months, echocardiography and chest radiography were performed to check for pneumothorax, pericardial effusion reaccumulation, or the appearance of pleural effusion after pigtail catheter removal. Main results The procedure was successful and without recurrence in 44 patients (88%). Procedural complications were fever in 4 patients (33%) and 10 patients (26%) in group 1 and group 2, respectively (p = 0.72), and mild pneumothorax in 2 patients (17%) and 1 patient (3%) in group 1 and group 2, respectively (p = 0.14). Fifty percent of the patients died within 4 months, while 25% survived to 11 months. High serum calcium, a low albumin/globulin ratio, and positive results on pericardial effusion cytology were poor prognostic factors for long-term survival. Conclusion Both immediate and delayed DBP are a safe and effective method of relieving large pericardial effusions in patients with cancer. Successful DBP without recurrence of pericardial effusion was achieved in 88% of all patients. Survival was related to the extent of the disease.

A large renal arteriovenous fistula (RAF) may lead to heart failure, renal insufficiency, hematuria, and progressive increase in size of renal vessels. Here we present the case of a 67-year-old man with a huge left RAF, who suffered from exertional dyspnea, nocturnal orthopnea, and impaired renal function. The left renal vein and inferior vena cava were dilated to 4 cm. An Amplatzer Vascular Plug with the largest size of 30 mm in disk diameter was deployed to block the fistula, with balloons inflated at renal artery and vein in advance, to reduce the renal flow in order to prevent plug migration. The decrease of shunt flow after embolization was suboptimal. However, dyspnea ameliorated, which was associated with decreased cardiac murmur, subsided abdominal bruit, normalization of the lowered diastolic pressure, and better renal function. In addition, more microcoils can be applied, using the lodged plug as a framework, to achieve the best clinical improvement.

Amyotrophic lateral sclerosis (ALS) is a motor neuron disease involving both the upper and lower motor neurons in the brain stem and spinal cord. Although it is well known that various central nervous system disorders can produce a ‘pseudo-infarction’ pattern on the electrocardiogram, there have been no reports of this particular pattern in ALS patients. This report concerns an ALS patient who presented with an ECG pattern of S–T elevation followed by biphasic T and inverted T without any detectable myocardial abnormality. Data from the present case suggest that this pattern may be an inherent characteristic of ALS.

Aims: To evaluate the correlation of the flow patterns of the four pulmonary veins as assessed by transesophageal echocardiography and the influence of significant mitral regurgitation on this correlation. Methods and Results: Eighty-eight patients with normal sinus rhythm and variable underlying cardiovascular diseases underwent transthoracic and transesophageal echocardiographic studies. Doppler flow of the four pulmonary veins could not be adequately interpreted in 19 patients (22%). The left atrial dimension of these patients was significantly larger than that of the patients with complete study of the flow in the four pulmonary veins (49 ± 6 vs. 43 ± 7 mm; p < 0.05). Of the 69 patients with complete evaluation of the four pulmonary veins, 48 patients without significant mitral regurgitation were analyzed as group A, and the remaining 21 patients as group B. The peak systolic and diastolic forward flow velocities of the four pulmonary veins were measured and the ratio of peak systolic (S) to diastolic (D) flow velocity was calculated. Group A had a significantly larger S/D ratio in all four pulmonary veins than group B (p < 0.05 in each pulmonary vein measurement). There was good correlation of the flow pattern represented as S/D ratio between left upper and lower pulmonary veins (r = 0.90) and between right upper and lower pulmonary veins (r = 0.89) in group A. The correlation of the flow pattern among the four pulmonary veins deteriorated in group B. Conclusion: Pulmonary veins on the same side share rather similar flow patterns in comparison with pulmonary veins on the opposite sides. The correlation of flow patterns among the four pulmonary veins is good in subjects without significant mitral regurgitation, but it worsens in patients with significant mitral regurgitation. Therefore, cautious interpretation of flow patterns of the four pulmonary veins in patients with significant regurgitation is indicated for grading the severity of mitral regurgitation.

The angiotensin-converting enzyme (ACE) gene product plays an important role in cardiovascular homeostasis. An insertion/deletion (I/D) polymorphism in intron 16 of the ACE gene, with insertion polymorphism containing three more Alu-repeat sequences, was reported to be a determining factor of the plasma ACE concentration, and the D polymorphism has been found to be associated with certain cardiovascular diseases (1)(2)(3)(4)(5). Controversy exists, however, regarding the strength of the association. The diversity of conclusions has been attributed to methodological and technical variations in detection of the polymorphisms (6)(7). The preferential amplification of the D allele of the ACE gene by the PCR reported by Rigat et al. (8) was thought to be one cause. This PCR method occasionally mistyped ID heterozygotes as DD homozygotes (9). The probability of this mistyping has been estimated to be ∼5–10% (6)(7). A confirmatory PCR method, which requires an additional third PCR primer inside the Alu sequence of the I allele, was proposed to minimize the mistyping of the I allele as a D allele (9). Although this PCR technique was reported to be 100% in the typing of ACE gene polymorphisms, problems with the preferential amplification of multiplexed PCR are not entirely excluded with this method (10)(11). A stepdown PCR method, modified from touchdown PCR, has recently been used in several molecular studies (12). This method involves initial PCR annealing temperatures higher than the melting point of the primers, followed by annealing temperatures reduced stepwise to the melting point. This method should result in higher amplification specificity and greater yield. We compared the stepdown PCR with the conventional method from Rigat et al. (8) and with confirmatory PCR in the amplification efficiency of the ACE gene. We collected blood samples from …

Surgical treatment for atrial fibrillation is now feasible in selective cases. The aim of this study was to assess the electrophysiological properties of patients undergoing atrial compartment operation for chronic atrial fibrillation.Electrophysiological studies were performed in 20 mitral valve patients with atrial fibrillation who had been maintained in sinus rhythm for more than 1 year after atrial compartment operation. Intra-cardiac recording and programmed electrical stimulation were performed in various atrial compartments. The parameters studied included sinus node function, atrial conduction and refractoriness, atrioventricular conduction function and inducible arrhythmias if any. Intra-cardiac recordings showed that the rhythm was of sinus origin in all cases, with the earliest atrial activity located in the high right atrium. The mean sinus cycle length was 750 +/- 110 ms, AH time 106 +/- 29 ms, and HV time 53 +/- 7 ms. The sinus node function was normal in 18 patients (90%), and only two patients had prolonged sinus node recovery and sino-atrial conduction. The right atrial appendage compartment was driven by the sinus node in all patients. However, the conduction time from the high right atrium to the right atrial appendage compartment was markedly prolonged in 12 of 15 patients (80%) undergoing the three-compartment operation in which an incision was placed between the high right atrium and right atrial appendage compartments. On the other hand, the electrical activities in the left atrial compartment were much more varied. In 13 of 20 patients (65%), the left atrial compartment was driven by the sinus node; 11 of the 13 patients had a normal or mildly prolonged conduction time (ranged 75 to 146 ms), whereas two patients had a marked delay in conduction (200 ms and 266 ms, respectively). In the remaining seven patients, the left atrial compartments were dissociated from the rest of the heart; five of them had a quiescent left atrium, one a fluttering left atrial rhythm, and one a slow left atrial rhythm. The effective refractory period was longer in the left atrial compartment (242 +/- 47 ms) as compared to that of the high right atrium (224 +/- 26 ms, P0.01) and right atrial appendage compartments (219 +/- 25 ms, P0.01). Programmed electrical stimulation could not induce atrial fibrillation in any patient, whereas two patients had inducible atrial flutter and three repetitive atrial responses.(1) Atrial compartment operation does not impair sinus node function in most cases. (2) Elimination of atrial fibrillation while maintaining the electrical connection between different atrial compartments is feasible.

We investigated the intrinsic cardiac mechanics of myocardium and changes in titin in insulin-resistant rats. Microsonometry and micromanometry were used to evaluate the maximal elastance (Emax) and myocardial stiffness constant (Km) of the left ventricle, in addition to the traditional systolic and diastolic cardiac function, with an isolated working heart preparation. Thirty 150 g Wistar rats were divided into three groups of 10. Group A was fed rat chow, while groups B and C were fed a 66% fructose diet for 7-8 months. Group C also received clonidine. Group B rats developed insulin resistance, as well as elevated plasma glucose and blood pressure. Group C rats also had insulin resistance and elevated plasma glucose, but not higher blood pressure. Group B rats had decreased Emax, decreased peak-dp/dt, prolonged Tau and increased Km compared to normal control rats. Group C rats, which mimicked the clinical condition of diabetic cardiomyopathy, maintained normal global left ventricular function as revealed by cardiac output, peak + dp/dt, peak-dp/dt and Tau of relaxation. However, they had a lower Emax slope (355 +/- 51 vs 535 +/- 56 mmHg.mm than group A rats, p0.05) and increased Km (81.6 +/- 9.9 vs 25.5 +/- 4.8 in group A, p0.001), even though the extent of elevation of plasma glucose was only mild (71.3 +/- 2.0 to 108.9 +/- 4.4 mg/dl, p0.001). Their left ventricular mass, myocyte size, interstitial fibrosis and vascular picture did not change. However, the content of myocardial titin decreased significantly (intensity ratio of titin/actin was 0.23 +/- 0.01 and 0.29 +/- 0.02 in group C and group A rats respectively, p0.05). These findings suggest that changes in titin play a role in the change in myocardial functional characteristics and may be one of the causes of diabetic cardiomyopathy.

To investigate the mechanism of sympathovagal imbalance due to myocardial ischemia, we studied 42 consecutive patients undergoing successful percutaneous transluminal coronary angioplasty by correlating frequency domain and time domain measures of heart rate variability with parameters such as echocardiography, stress thallium scanning and radionuclide angiography before, immediately after and 2 months after the procedure. Of these, 20 patients (Group N) had normal and 22 patients (Group A) had abnormal regional wall motion. A control group of 20 healthy subjects (Group C) underwent echocardiography and examination of heart rate variability twice at 2-month intervals to check for spontaneous variations. At baseline, frequency domain measures such as low and high frequency power and time domain measures such as SDANN index (the mean of the standard deviations of the average of RR intervals) were lower in Group A than in Groups N and C, whereas no differences were detectable in ultra low and very low frequency, total power, SDNN index (the mean of the standard deviations of the mean of normal RR intervals), and r-MSSD (the root mean square of successive RR differences). There was high association between the diastolic wall stress index and both high frequency (r = -0.82) and low frequency power (r = -0.77). There were similar findings for the systolic wall stress index (r = -0.72 for high frequency and r = -0.64 for low frequency power). After successful coronary angioplasty, regional wall motion, left ventricular wall stress indices and all measures of heart rate variability were unchanged in Group N. In Group A the mean summed segment score improved from 15.9 +/- 2.6 to 12.2 +/- 1.7 (p0.0001), and mean low frequency, mean high frequency power (logarithmic units), and SDANN index (msec) increased from 6.10 +/- 0.23 to 6.36 +/- 0.28 (p0.005), from 5.36 +/- to 0.40 to 5.70 +/- 0.39 (p0.01) and from 70 +/- 18 to 83 +/- 18 (p0.01) respectively. In addition, low and high frequency power and SDANN index, lower at baseline in Group A than in the other two groups, were comparable in the three groups after coronary angioplasty. The evolution of diastolic and systolic wall stress indices paralleled that of the above three parameters. In conclusion, diastolic and systolic wall stress indices, in addition to segmental left ventricular dysfunction, were synergistically involved in determining sympathovagal imbalance in patients with significant coronary artery disease; the reversal of left ventricular dysfunction and wall stress indices improves the profile of heart rate variability. Alterations in cardiac geometry and wall stress influence mainly the discharge of afferent sympathetic and efferent parasympathetic innervations and also principally the long-term heart rate variations instead of short-term modulation.

Atrial fibrillation (AF) has been reported as an independent risk factor of systemic thromboembolism. Almost half of the left atrial thrombi are located in the left atrial appendage (LAA). LAA function, reflected by LAA flow, thus has an influence on the potential of distal embolic complications. To identify factors other than atrial contraction that influence LAA flow during AF, transthoracic and transesophageal echocardiographic studies were performed on 130 patients. Seventy patients with nonrheumatic AF were divided into two groups with higher peak LAA outflow velocity (group 1) and lower peak LAA outflow velocity (group 2) at the ventricular systolic phase. Sixty patients with rheumatic AF were classified as group 3. Group 1 had a higher peak LAA outflow velocity than group 2 at both the ventricular systolic and diastolic phases. Group 2 had a higher peak LAA outflow at the ventricular diastolic phase than group 3 (18.9 +/- 8.0 vs. 11.8 +/- 7.5 cm/s, p0.001), whereas there was no significant difference in the peak LAA outflow at the ventricular systolic phase between the two groups (9.6 +/- 4.0 vs. 10.8 +/- 6.8 cm/s, p = NS). Group 3 was subdivided according to mitral valve area. Patients with severe mitral stenosis (mitral valve area1 cm2) had a significantly lower diastolic augmentation of LAA outflow velocity (difference of LAA outflow velocity between ventricle systole and diastole) than patients with mild to moderate stenosis (0.5 +/- 3.2 vs. 2.6 +/- 4.9 cm/s, p0.05). In conclusion, patients with rheumatic AF, especially those with severe mitral stenosis, have a lower diastolic augmentation of LAA outflow velocity. The lower diastolic augmentation of the LAA outflow velocity at the ventricular diastolic phase might result from interference with the suction effect of the left ventricular diastole by the stenotic mitral valve.

To assess the correlation of pulmonary venous flow pattern with the magnitude of the dynamic change in left atrial pressure (i.e. x and y descents) and to elucidate the way how pulmonary venous flow pattern reflects left atrial pressure, we studied 35 patients with normal sinus rhythm undergoing transesophageal echocardiography and cardiac catheterization. The ratio of peak systolic/diastolic flow correlated well with the ratio of x/y descent (r = 0.88) and the ratio of systolic/diastolic velocity-time integral (r = 0.89). The correlation between the ratio of systolic/diastolic flow or velocity-time integral and mean atrial pressure was less strong (r = -0.49 and -0.70, respectively). We conclude that the ratio of peak systolic/diastolic flow velocity, or the ratio of systolic/diastolic velocity-time integral of pulmonary venous flow reflects the phasic change in left atrial pressure more appropriately than the mean left atrial pressure. Due to the good correlation between the phasic change in left atrial pressure and pulmonary venous flow pattern, the flow pattern of pulmonary veins could be used to identify diseases with specific patterns of left atrial pressure.

Clinical decisions and controlled studies in regard to hypertension have long emphasized the casual diastolic blood pressure (DBP). The influence of superimposition of high systolic blood pressure (SBP) on the target organ damage has been less studied. To assess the role of isolated diastolic hypertension without interference of superimposition of systolic hypertension, 171 subjects with normal blood pressure, isolated diastolic hypertension (SBP140 and DBPor = 90 mmHg) isolated systolic hypertension (SBPor = 140 and DBP90 mmHg) or combined hypertension (SBPor = 140 and DBPor = 90 mmHg) determined by mean 24-h ambulatory blood pressure were compared in relation to target organ damage including ECG abnormality related to hypertension, cardiac enlargement by chest X-ray, proteinuria and retinopathy. The incidence of target organ damage was lower in subjects with normal BP than in the other three groups. The incidence of target organ damage was almost significantly higher in patients with isolated systolic hypertension than in those with isolated diastolic hypertension. No significant difference in the incidence of complications existed between patients with isolated systolic and combined hypertension. These findings demonstrate that the severity of hypertensive complications is more closely related to mean ambulatory SBP than mean ambulatory DBP. The level of systolic BP is important for predicting the severity of target organ damage in patients with high diastolic BP, because there is a significant difference in the incidence of target organ damage between isolated diastolic hypertension and combined hypertension.

BACKGROUND: Ischemic mitral regurgitation (IMR) is common in ischemic heart disease and results in poor prognosis. However, the exact mechanism of IMR has not been fully elucidated. HYPOTHESIS: Quantitation of the mitral tetrahedron using three‐dimentianl (3D) echocardiography is capable of evaluating the geometric determinants and mechanisms of IMR. METHODS: Forty patients with a history of ST‐elevation myocardial infarction at least 6 months earlier were studied. Parameters of mitral deformation and global left ventricular (LV) function and shape were evaluated by 2‐dimensional echocardiography. The effective regurgitant orifice (ERO) of IMR was obtained by the quantitative continuous‐wave Doppler technique. Three‐dimensional (3D) echocardiography was applied to assess the mitral tetrahedron. RESULTS: Mitral valvular tenting area (P

To study the correlation between ambulatory blood pressure and target organ complications of hypertension, ambulatory blood pressure monitoring was performed on 290 patients with mild to moderate essential hypertension before treatment. Their target organ complications of hypertension were assessed by ECG, chest X-ray, urinalysis and an eye-fundus examination. An average ambulatory diastolic blood pressure value greater than the casual diastolic blood pressure was found in 35% of subjects with ECG evidence of left ventricular hypertrophy (LVH) and 5. 2% of subjects without (P

Body surface potential maps were obtained in 50 normal adults using the heart potential map system designed by Yamada. Group A (younger adult group) consisted of 30 persons whose ages ranged from 20 to 39 years. Group B (middle-aged group) included 20 persons whose ages ranged from 40 to 59 years.Although there were slight variations in the pattern of isopotential distribution among the subjects studied, a consistent pattern with a similar sequence was observed in both study groups. However, there were some parameters which significantly differed between groups A and B, including the earliest appearance time of the anterior negative potential (p

Recent investigation has demonstrated that prostaglandin E(1) (PGE(1)) therapy increased capillary density in explanted hearts. Dynamic (13)N-ammonia positron emission tomography (PET) is reliable for non-invasive measurement of myocardial blood flow and myocardial perfusion reserve (MPR). The aim of this study was to investigate the effects of PGE(1) therapy during 4 weeks on reduction of myocardial perfusion abnormalities and increase of MPR in the patients with ischemic heart disease.In this double-blind, placebo-controlled trial, we randomly assigned 11 patients who had symptomatic heart failure and documented myocardial ischemia to 4 weeks intravenous infusion of PGE(1) (2.5 ng/kg/min; 8 patients, age 60 ± 13 years) or saline (3 patients, age 57 ± 13 years). Dynamic (13)N-ammonia PET scans at rest and during adenosine stress were obtained at baseline and 12 weeks after treatment completion. Quantitative size/severity of perfusion defects and MPR change from baseline to follow-up PET were determined using a 17-segment model.Compared with the control group, baseline MPR in the PGE(1) group was significantly lower (1.96 ± 0.78 vs. 2.71 ± 0.73; P 0.001). MPR significantly improved 12 weeks after completion of PGE(1) infusion (1.96 ± 0.78 to 2.16 ± 0.77; P 0.001). In contrast, MPR declined significantly in the placebo group (2.71 ± 0.73 to 2.01 ± 0.58, P 0.001).Four weeks of PGE(1) infusion sustained MPR improvement in patients with ischemic heart disease. This may be an attractive therapeutic approach for no-option patients with severe ischemic cardiomyopathy.

We compared the haemodynamic and metabolic effects of acetyl-L-carnitine (one of the carnitine derivatives) and of oxfenicine (a carnitine palmitoyltransferase-1 inhibitor) in streptozotocin-induced diabetes in male Wistar rats.Diabetes was induced by a single tail vein injection of 55mgkg(-1) streptozotocin. The diabetic animals daily treated with either acetyl-L-carnitine (150mgkg(-1) in drinking water) or oxfenicine (150mgkg(-1) by oral gavage) for 8weeks,were compared with the untreated age-matched diabetic controls. Arterial wave reflection was derived using the impulse response function of the filtered aortic input impedance spectra. Thiobarbituric acid reactive substances (TBARS) measurement was used to estimate malondialdehyde (MDA) content.Oxfenicine, but not acetyl-L-carnitine, increased total peripheral resistance in diabetes, which paralleled its elevation in plasma levels of free fatty acids. By contrast, acetyl-L-carnitine, but not oxfenicine, resulted in a significant increase in wave transit time and a decrease in wave reflection factor, suggesting that acetyl-L-carnitine may attenuate the diabetes-induced deterioration in systolic loading condition for the left ventricle. This was in parallel with its lowering of MDA/TBARS content in plasma and aortic walls in diabetes. Acetyl-L-carnitine therapy also prevented the diabetes-related cardiac hypertrophy, as evidenced by the reduction in ratio of the left ventricular weight to body weight. Acetyl-L-carnitine, but not oxfenicine, attenuates aortic stiffening and cardiac hypertrophy, possibly through its decrease of lipid oxidation-derived MDA/TBARS in the rats with insulin deficiency.

The aim of this study was to examine the effect of surgical weight reduction on cardiac structure and function and to seek the determinants of these changes. Sixty-six severely obese adults (BMIor=35 kg/m(2)) who received bariatric surgery underwent echocardiographic examination before and 3 months after surgery. At 3 months after surgery, BMI and systolic blood pressure (BP) decreased (43.3 +/- 6.3 to 34.1 +/- 5.6 kg/m(2), P0.001, and 146 +/- 12 to 130 +/- 14 mm Hg, P0.001, respectively). In left ventricular (LV) geometry, the relative wall thickness (RWT) and LV mass index decreased significantly (0.43 +/- 0.05 to 0.35 +/- 0.05, P0.001, and 50 +/- 11 to 39 +/- 11 g/m(2.7), P0.001, respectively) without changes in chamber size. Multivariate analyses showed change in systolic BP to be an independent predictor for the changes in RWT and LV mass index. In myocardial performance, peak systolic mitral annular velocity and all diastolic indexes showed significant improvements. We concluded that LV hypertrophy and function improved rapidly after bariatric surgery in severely obese adults. BP reduction was the major determinant for the regression of LV hypertrophy in the early stage of surgical weight reduction.

[Figure][1] [![Graphic][3] ][3][![Graphic][4] ][4] A 37-year-old woman with Marfan's syndrome underwent a modified Bentall's operation with the coronary button technique in 2007. Eight months later, she presented with non–ST-segment elevation myocardial infarction with the

Background: Studies have demonstrated that improvement in cardiovascular risk factors may contribute to reduced coronary artery disease (CAD) morbidity and mortality, improved patient outcomes, and lower medical costs associated with treating heart disease. Purpose: The purpose of this study was to understand the coronary risk factor profile, to have the knowledge of risk factors, to understand the modifying behaviors, and to understand the factors associated with modifying behaviors of cardiovascular risk factors among patients with CAD in northern Taiwan. Methods: A cross-sectional design was used in this study. Using nonprobability sampling, 156 patients diagnosed with CAD were interviewed and asked to complete a structural questionnaire in cardiovascular clinics at three medical centers in northern Taiwan. Data were analyzed by descriptive analysis, Pearson's correlation, chi-square tests, and stepwise multiple regression. Results: A total of 38% of variance of modifying behaviors was explained by self-efficacy, actual risk factors, work status, and health beliefs. Self-efficacy was the strongest predictor of behavior to modify cardiovascular risk factors. Age and type ”A” personality were the two leading cardiovascular risk factors for the participants. Most participants could perform modifying behaviors such as taking medications, eating an appropriate diet, and following specific lifestyle recommendations. However, participants had relatively lower adherence to monitoring blood pressure, exercising regularly, and controlling weight. Conclusions/Implications for Practice: Nurses should assess patient cardiovascular risk factors, health beliefs, and self-efficacy and then provide comprehensive and adequate instruction to each based on his or her specific risk factors.

Background This study was designed to evaluate the joint effects of plasma C-reactive protein (CRP) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) vs coronary angiographic severity on cardiovascular risk stratification. Methods and Results A total of 345 patients with stable coronary artery disease (CAD) were recruited after successful percutaneous coronary intervention (PCI). Endpoints were major adverse cardiovascular events (MACE) and cumulative clinical restenosis rate after 18-36-month follow-up. Plasma NT-proBNP and CRP levels were among the strongest predictors of MACE. Adjusted hazard ratios of MACE according to combined biomarkers were 2.4 (p=0.05) for elevated CRP only, 5.22 (p

In an effort to enlarge the clinical application of body surface potential maps (BSPMs), the authors studied the relationship between abnormal ventricular wall motion and BSPMs in 98 consecutive patients with angiographically proven coronary artery disease (CAD). Forty-nine of the patients (50%) had wall motion abnormalities as seen on single-plane left cine ventriculograms. During early ventricular depolarization, normal BSPMs have a potential maximum that is greater than the absolute value of the potential minimum; this reverses in late depolarization such that the absolute value of the potential minimum is the greater. The patients showed a significantly early reversal (p less than 0.001), and 55 (56.1%) had abnormal "early reversal" BSPMs. This abnormal "early reversal" is closely related to abnormal ventricular wall motion. Using it as an indicator of abnormal wall motion, the authors obtained the sensitivity, specificity, positive predictive value, and negative predictive value of the following conditions: LAD lesions, LCX, RCA, LAD and RCA lesions, LAD and LCX, and three-vessel disease, and for all patients. A relatively high sensitivity (85%) and specificity (80%) was found in patients with LAD lesions only or multivessel lesions in addition to LAD lesions.