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The mechanism of cardiac rupture after MI (myocardial infarction) is not fully understood. Rupture has not been reported in most laboratory species, including the rat, but does occur in mice. We have reported previously that β2-TG mice (transgenic mice with cardiac-restricted overexpression of β2-adrenergic receptors) had a lower incidence of rupture compared with NTG (non-transgenic) littermates. We hypothesized that the difference in the incidence of rupture between rodents and specific mouse strains is due to the difference in collagen content following MI. In the present study, we compared the difference in matrix remodelling post-MI between β2-TG and NTG mice and between mice and rats. MI was induced by ligation of the left main coronary artery. Following MI, tensile strength, insoluble and soluble collagen content and gelatinase expression were determined in the infarcted and non-infarcted myocardium. Better preserved tensile strength measured as TTR [tension-to-rupture; 88±14 and 58±3% of the respective sham group values for β2-TG compared with NTG mice (P

Cardiac rupture remains a fatal complication of acute myocardial infarction (MI) with its mechanism partially understood. We hypothesized that damage to the collagen matrix of infarcted myocardium is the central mechanism of rupture and therefore responsible for the difference in the incidence of rupture between genders. We examined left ventricular (LV) remodeling during the acute phase post-MI in 129sv mice. Following induction of MI, we monitored rupture events and assessed the extent of LV remodeling by echocardiography. Muscle tensile strength, content of insoluble and soluble collagen, expression and activity of matrix metalloproteinases (MMPs) and density of inflammatory cells were determined in the infarcted and non-infarcted myocardium. We then tested the effects of MMP inhibition on rupture. Compared to female mice, males with MI displayed greater extent of LV remodeling, reduced muscle tensile strength, loss of insoluble collagen, local inflammatory response and MMP-9 activation, changes associated with a 3 times higher incidence of rupture than in females. MMP-9 expression by circulating blood mononuclear cells was also increased in male mice with acute MI. Treatment of male mice with an MMP inhibitor reduced MMP activity and halved rupture incidence. Our findings demonstrate that the differences in the severity of inflammation, MMP activation and damage to collagen matrix account for gender difference in cardiac rupture. Our study illustrates the breakdown of fibril collagen as a central mechanism of cardiac rupture.

The purpose of this study is to demonstrate safety and effectiveness of the S-Stent in de novo coronary lesions treated with conventional percutaneous coronary balloon angioplasty. Between January 2000 and June 2001, 120 patients were prospectively enrolled at four study centers. Patients were treated with coronary stenting in a total of 137 lesions. Procedural success was achieved in 100% of 137 attempted lesions. Clinical success was 99.8%. In-hospital mortality was 0.8%; myocardial infarction occurred in 0.8% and stent thrombosis in 0.8%. After stent implantation, the minimal lumen diameter increased from 0.92 ± 0.43 to 2.74 ± 0.36 mm (P < 0.0001) and the percent diameter stenosis decreased from 68.0 ± 16.2 to 4.5 ± 12.0 (P < 0.0001). At 6-month follow-up, the percent diameter stenosis was 33.5 ± 21.3 and the angiographic restenosis rate was 16.5%. Target lesion revascularization was required in 12 patients (10.1%). We conclude that the use of S-Stent for coronary intervention resulted in a high procedural success rate and low angiographic restenosis at 6 months after implantation. Catheter Cardiovasc Interv 2004;62:439–444. © 2004 Wiley-Liss, Inc.

We conducted a randomized feasibility pilot study comparing combined fibrinolysis with immediate rescue angioplasty vs. primary angioplasty with adjunctive abciximab in patients with acute myocardial infarction (AMI). Seventy patients with ST segment elevation AMI of ≤ 6 hr were randomized to either 50 mg of alteplase and abciximab (n = 34) or primary angioplasty with adjunctive abciximab (n = 36). Coronary angiography was performed at 60 min in the combined lytic group and TIMI 3 flow was present in 65% of patients as compared to 25% (P = 0.001) in the primary angioplasty group prior to intervention. Treatment success, defined as TIMI 3 flow, was achieved in 83% of patients in the primary angioplasty group (P = 0.075 compared to 65% in combined lytic group before rescue angioplasty). There was no difference in overall treatment success between primary angioplasty and combined lytic group with rescue angioplasty (83% vs. 94%; P = NS). Major adverse cardiac events at 1 month were not significant (15% vs. 11%; P = NS), but there was a trend toward more events in the combined lytic group at 6 months (32% vs. 14%; P = 0.066), particularly in target vessel revascularization. In this feasibility pilot study, high rate of TIMI 3 flow was attained in patients with AMI with both combined fibrinolysis and primary angioplasty with adjunctive abciximab. A larger randomized trial is currently ongoing to compare these two strategies. Cathet Cardiovasc Intervent 2004;62:445–452. © 2004 Wiley-Liss, Inc.

Aim: The purpose of this report is to survey the factors contributing to variation in lipoprotein(a) (Lp(a)) in a population-based sample of Anglo-Celtic Melburnians. Results: The plasma Lp(a) levels were highly skewed towards low levels in this population, with a median of 156 mg/l and a mean of 262 mg/l. Approximately 33% had plasma Lp(a) above the threshold value of 300 mg/l, while 35% had Lp(a) levels below 100 mg/l. The most commonly occurring phenotype was apo(a) S3. In this phenotype, Lp(a) concentrations ranged from 10 to 596 mg/l. Lp(a) was consistently associated with diastolic blood pressure, systolic blood pressure, total protein, albumin and nitrogen excretion in the 40–60 y age group. Multiple stepwise regression analyses, in non-dietary factors, were used to explain about 13% of the variance in Lp(a) (19% in men and 23% in women). Remarkably, in the

The aim of this study is to determine whether the tyrosine kinase plays a role in the contractile response of human radial artery (RA), internal mammary artery (IMA) and saphenous vein (SV) to alpha(1)-adrenoceptor (AR) stimulation. The tyrosine kinase inhibitors, genistein and tyrphostin, significantly inhibited alpha(1)-AR mediated contractile response in a dose-dependent and non-competitive manner. Genistein at 10 microM inhibited 39%, 54% and 72% of PE-induced maximum contraction, and tyrphostin at 50 microM inhibited 41%, 68% and 39% of the contraction in the human RA, IMA and SV respectively. These results suggest that tyrosine kinases participate in regulation of signal transduction that is associated with alpha(1)-AR mediated contractile response in human blood vessels.

The factors contributing to variation in lipoprotein(a) [Lp(a)] was studied in a Melbourne Chinese population. The plasma Lp(a) levels were highly skewed towards low levels in this population, with a median of 79 mg/L and a mean of 145 mg/L. Approximately 13% had plasma Lp(a) above the threshold value of 300 mg/L, while 57% had Lp(a) levels below 100 mg/L. The most commonly occurring phenotype was apolipoprotein(a) )] S4 which is usually inversely correlated with plasma Lp(a) levels but not S1 and S2, which are usually with higher levels of Lp(a). In this phenotype, Lp(a) concentrations ranged from 4 to 228 mg/L. The positive association of Lp(a) levels with BMI and LDL cholesterol was observed in women and men, respectively. Taken together, these observations indicate that the Lp(a) genotype, and its expressed phenotype, in Chinese may offer protection against CHD, unless in women there is an associated increase in BMI, and in men an associated increase in LDL. The stepwise regression analyses showed that in those over 60 years of age, about 29% of the variance of in Lp(a) was explained by diet and 12% by non-dietary factors. Thus, the apo(a) phenotypes clearly influence Lp(a) concentrations, but are not the only factors, which determine the variation in Lp(a) concentrations, environmental or other biochemical factors may contribute to Lp(a) status.

1. To determine the effects of trace elements on alpha1-adrenoceptor-mediated vasoconstriction, we studied the effects of molybdenum (Mo), silicon (Si) and nickel (Ni) on vasoconstrictor response to an alpha1-adrenoceptor agonist in rat aorta. 2. Cumulative concentration-contraction curves were obtained for phenylephrine (1 nmol/L-10 micromol/L) in the absence and presence of Mo, Si and Ni (0.3, 1 and 3 micromol/L) in rat aorta rings. Increasing the concentration of Mo and Si from 0.3 to 3 micromol/L shifted the cumulative concentration-contraction curve to the right, but did not reduce the maximal contractile response to phenylephrine. In contrast, Ni at 1 and 3 micromol/L shifted the cumulative concentration-contraction curve to the right and, at 3 micromol/L, reduced the maximum contractile response to phenylephrine. 3. We conclude that micromolar concentrations of Mo, Si and Ni affected alpha1-adrenoceptor-induced vasoconstriction and that Ni significantly inhibited the maximal contractile response to phenylephrine in rat isolated aorta.

The purpose of this study was to determine the impact of these 2 reperfusion strategies (reduced-dose alteplase plus abciximab or direct angioplasty plus abciximab) on fibrinolytic and thrombin generation activities. The effect of reduced-dose alteplase plus abciximab and direct angioplasty plus abciximab on hemostatic factors is unknown. Of 70 patients with acute myocardial infarction ofor = 6 hours, 34 were randomized to reduced-dose alteplase (35 to 50 mg in 1 hour) and 36 to direct angioplasty. A standard bolus and infusion dose of abciximab was administered to all patients. Blood specimens were collected at baseline, and at 1, 4, 12, and 24 hours. The following parameters were assayed: fibrinogen, plasminogen and antiplasmin activities, tissue plasminogen activator antigen, D-dimer, prothrombin fragments F1 + 2, and thrombin/antithrombin III complexes. Among patients treated with reduced-dose alteplase plus abciximab, the fibrinogen level decreased by 28.4% in the first hour (11.7 +/- 3.4 vs 7.8 +/- 2.5 micromol/L, p0.001). Correspondingly, plasminogen and antiplasmin activities decreased by 43.8% (p0.001) and 59.1% (p0.001), respectively. Prothrombin fragments F1 + 2 increased from 2.2 +/- 1.7 to 4.2 +/- 1.6 nmol/L (1 hour) (p0.001) and thrombin/antithrombin III increased from 16.3 +/- 15.0 to 33.5 +/- 19.9 microg/L (1 hour) (p0.001). Conversely, in the direct angioplasty group, there was a marginal elevation in fibrinogen level at 1 hour (10.2 +/- 2.4 vs 10.6 +/- 2.0 micromol/L, p = 0.064) despite a significant reduction in plasminogen and an increase in tissue plasminogen activator levels. There was no significant change in prothrombin fragments F1 + 2 and thrombin/antithrombin III levels. Thus, there was considerable fibrinolytic activity with reduced-dose alteplase plus abciximab; thrombin generation was not prevented. Among patients treated with direct angioplasty, there was some endogenous fibrinolytic activity, but there was no significant thrombin generation.

In this study we analyzed the different alpha1-adrenoceptor (AR) subtypes present in human saphenous vein (HSV) using reverse transcription polymerase chain reaction (RT-PCR), DNA-DNA hybridization analysis and functional affinities for alpha-AR antagonists. DNA-DNA hybridization analysis of RT-PCR amplification products confirmed the presence of alpha1A- and alpha1B-ARs, and low levels of alpha1D-AR in HSV. The functional results showed: (1) prazosin, the selective alpha1-AR antagonist, phentolamine, the alpha1- and alpha2-ARs antagonist, WB 4101 and 5-MU, the selective alpha1A-AR subtype antagonists were potent, competitive antagonists of noradrenaline (NA)-induced contraction (pA2 values of 11.03, 8.06, 9.02 and 8.34, respectively). (2) Alpha1-AR-induced contraction was sensitive to the alkylating effects of CEC (the alpha1B and alpha1D-AR subtypes antagonist) and (3) The selective alpha1D-AR subtype antagonist BMY displayed low affinity (pA2 values of 6.44). This indicates that the contractile response of the HSV to alpha1-AR-induced is predominantly mediated by both alpha1A and alpha1B-AR subtypes. This was also supported by the good relationship between pA2 values from the present study and reported binding affinities (pKi) values of various alpha1-AR subtype antagonists with cloned human alpha1A- and alpha1B-AR subtypes (r=0.89 and r=0.98, respectively), but not the alpha1D-AR subtype (r=0.67). Our results indicate that alpha1A- and alpha1B-ARs are the main functional and expressed receptor subtypes in HSV.

To determine the influences of the Mn, Cu, and Zn on α1-adrenoceptor (AR)-mediated vasoconstriction, we investigated their effects on vasoconstriction produced by the α1-AR agonist phenylephrine in isolated rings of rat thoracic aorta. The cumulative concentration-contraction curves for phenylephrine were obtained in the absence and presence of Mn (0.3, 1, 3 µM), Cu (1, 10, 16 µM), and Zn (0.3, 1, 10 µM). Mn, Cu, and Zn each inhibited phenylephrine-mediated contraction in a dose-dependent manner. The maximal phenylephrine-induced contraction was significantly reduced by the pretreatment of the arterial rings with 10 and 16 µM Cu (p

Stenting lesions with favorable characteristics as required for inclusion in the STRESS/ BENESTENT trials have yielded superior results to that of PTCA alone. Results for less favorable lesions such as in small vessels, diffuse disease, ostial disease, and saphenous vein grafts are less well established. This review seeks to analyze available data for stent placement in this subset of non-STRESS/BENESTENT lesions.

Different stent designs have widely disparate characteristics that may exert a positive or negative impact on their early and mid-term outcomes. The MultiLink stent (Guidant/Advanced Cardiovascular Systems, Santa Clara, CA) is a new coronary stent with only very limited data. In this report, we examined the results of 50 consecutive patients treated with 57 premounted sheathless MultiLink stents in 53 native coronary arteries with reference diameter > or =2.7 mm. Successful stenting was achieved in 98% of patients, resulting in an improvement in diameter stenosis from 91%+/-11% to 1%+/-3% (P = 0.0001). At 1 month, there was no death, myocardial infarction, or stent thrombosis. Angiographic restudy at a mean of 5.0+/-1.8 months in 94% of patients revealed an in-stent restenosis rate of 20.7%. The restenosis rates for diabetic patients (vs. nondiabetic patients), type C lesions (vs. type A/B1 lesions), and the use of 35-mm-long stents (vs. 15-mm-long stents) were 45.4% (14.3%), 56% (< or =11%), and 80% (8.8%), respectively (P < 0.05). In conclusion, the present study demonstrates that the MultiLink stent has an excellent performance profile, is associated with a low risk of stent thrombosis in native coronary vessels, and yields a favorable restenosis rate, particularly after the use of short (15 mm) stents to treat simple lesions.

It remains controversial whether diabetes is associated with an increased risk of restenosis after intracoronary stenting.We selected 42 diabetic patients and an equal number of nondiabetic patients with follow-up angiographic restudy after single-vessel stenting, matched for 4 important stent-related and angiographic variables (stent design, reference vessel size and expanded stent diameter, coronary vessel treated, and poststent residual diameter stenosis). The 2 patient groups did not differ in their baseline lesion severity and acute luminal gain. At 5-month angiographic assessment, the observed in-stent restenosis rate was significantly higher in diabetic than nondiabetic patients (40.5% vs 16.7%, P = 0.0157). It was highest in diabetic patients who received small stents3.0 mm in diameter and intermediate in diabetic patients who received larger stent sizes (55% vs 27%, P = 0.0675). The frequency of restenosis in nondiabetic patients, however, was low; it was 18% and 15% in those who received small stents and larger stents, respectively (P = 0.7823).Our data suggest that diabetes predisposes to an increased risk of in-stent restenosis, particularly in small vessels.

We present a patient with Brugada-type ECG abnormalities and recurrent polymorphic ventricular tachycardia (VT). Subsequent investigations confirmed the diagnosis of isolated right ventricular myocardial infarction. The VT resolved after the 1st day and was not inducible subsequently. This case illustrates the importance of a careful study of the ECG to exclude other conditions in a patient with Brugada-type ECG abnormalities.

Objectives: We sought to develop a new quantitative method to evaluate the degree of myocardial perfusion. Background: Currently available methods for assessing myocardial perfusion, both TIMI myocardial perfusion grading (TMPG) and myocardial blush grading (MBG), are subjective. Methods: TIMI Myocardial Perfusion Frame Count (TMPFC), an objective method that measures the filling and clearance of contrast in the myocardium using cine-angiographic frame-counting, was developed to quantify myocardial perfusion. Myocardial perfusion of 45 normal coronary arteries in 15 patients, and 137 culprit arteries in 137 patients immediately after primary angioplasty, was successfully assessed with TMPFC. Results: The mean TMPFC in the normal arteries was 83.47 ± 17.96 frames (95% CI: 78.07 frames ≤ TMPFC ≤ 88.86 frames). Therefore, TMPFC < 90 frames, a value representing the upper bound of the 95% CI for the TMPFC observed in normal arteries, was defined as normal myocardial perfusion. In 137 culprit arteries, the mean TMPFC values after primary angioplasty for the right coronary artery (RCA), left anterior descending artery (LAD), and left circumflex artery (LCX) were 141 ± 82.6, 112 ± 80.3, and 102 ± 37.5 frames, respectively. Patients with suboptimal myocardial perfusion (ex: TMPG ≤ 2 or MBG ≤ 2 grade) had higher levels of TMPFC. Furthermore, multivariate analysis shows that the TMPFC was an independent predictor for 30-day (P = 0.0261) and 6-month incidence of MACE (P = 0.0207). Conclusions: TMPFC is a quantitative index for the assessment of myocardial perfusion; it allows quantification of TMPG and may serve as a discerning tool to predict prognosis in patients undergoing primary angioplasty. © 2009 Wiley-Liss, Inc.

Mitofusin-2 (Mfn2) suppresses smooth muscle cell proliferation through inhibition of the Ras-extracellular signal-regulated kinases (ERK1/2) pathway. Since the ERK1/2 pathway is implicated in mediating hypertrophic signaling, we studied the changes in Mfn2 in cardiac hypertrophy using in vitro and in vivo models. Phenylephrine was used to induce hypertrophy in neonatal rat ventricular myocytes (NRVMs). In vivo hypertrophy models included spontaneously hypertensive rats (SHR), pressure-overload hypertrophy by transverse aortic constriction (TAC), hypertrophy of non-infarcted myocardium following myocardial infarction (MI), and cardiomyopathy due to cardiac-restricted overexpression of beta(2)-adrenergic receptors (beta(2)-TG). We determined hypertrophic parameters and analysed expression of atrial natriuretic peptide (ANP) and Mfn2 by real-time PCR. Phosphorylated-ERK1/2 (phospho-ERK) was measured by Western blot. Mfn2 was downregulated in phenylephrine treated NRCMs (by approximately 40%), hypertrophied hearts from SHR (by approximately 80%), mice with TAC (at 1 and 3 weeks, by approximately 50%), and beta(2)-TG mice (by approximately 20%). However, Mfn2 was not downregulated in hypertrophied hearts with 15 weeks of TAC, nor in hypertrophied non-infarcted myocardium following MI. phospho-ERK1/2 was increased in hypertrophied myocardium at 1 week post-TAC, but not in non-infarcted myocardium after MI, indicating that downregulated Mfn2 may be accompanied by an increase of phospho-ERK1/2. This study shows, for the first time, downregulated Mfn2 expression in hypertrophied hearts, which depends on the etiology and time course of hypertrophy. Further study is required to examine the causal relationship between Mfn2 and cardiac hypertrophy.

Inflammation plays an important role in atherosclerosis. Markers of low-grade chronic inflammation, such as C-reactive protein (CRP) and soluble cell adhesion molecules (sCAMs), have been associated with coronary artery disease (CAD).To evaluate the significance of inflammatory markers as novel risk factors for CAD in the Chinese population.High-sensitivity CRP (hs-CRP); sCAMs, including vascular cell adhesion molecule-1 (sVCAM-1), intercellular cell adhesion molecule-1 (sICAM-1), P-selectin (sP-selectin) and E-selectin (sE-selectin); and white blood cell (WBC) count were measured in 170 angiographically defined CAD patients (70% or greater stenosis affecting at least one vessel) and 177 healthy control subjects in the Chinese population in Singapore.The levels of hs-CRP, sVCAM-1 and sP-selectin, and the WBC count were higher in CAD patients than in control subjects (P0.001, P0.05, P0.05 and P0.001, respectively). There were no significant differences in the levels of sICAM-1 and sE-selectin between the two groups. Patients with unstable angina or myocardial infarction had higher levels of hs-CRP, and higher WBC and monocyte counts than those with stable angina or atypical chest pain (all P0.05). The level of sP-selectin in patients with multivessel disease was higher than in those with single-vessel disease (P0.05). Overall, the levels of hs-CRP and sCAMs showed a significant correlation with the lipid profile and the WBC count.The present study suggests that inflammatory markers, including hs-CRP and WBC count, together with sP-selectin and sVCAM-1, could serve as markers of atherogenesis in Chinese patients with CAD, with potential diagnostic and therapeutic implications.

Objectives: Platelet-endothelial cell adhesion molecule-1 (PECAM-1) mediates the transendothelial migration of circulating leukocytes, a characteristic change in vascular inflammation leading to atherosclerotic plaque development. We hypothesized that genetic variation and soluble level of PECAM-1 could be associated with coronary artery disease (CAD). Design and methods: We analyzed two single nucleotide polymorphisms (SNPs) of PECAM-1 gene C+373G (Leu125Val) at exon 3, which encodes the first extracellular (Ig)-like domain that mediates the homophilic binding of PECAM-1, and G+1688A (Ser563Asn) at exon 8 in 144 angiographically documented (≥70% stenosis) patients with CAD and 150 age- and sex-matched controls in the Chinese population in Singapore, using a polymerase chain reaction–restriction fragment length polymorphism (PCR-RFLP) strategy. Level of plasma soluble PECAM-1 (sPECAM-1) was measured by ELISA. Results: The Leu125Val polymorphism was associated with CAD (P < 0.01). Also, the level of sPECAM-1 is was found to be elevated in CAD patients (P = 0.005). Moreover, subjects with the homozygous GG genotype of the Leu125Val polymorphism had higher sPECAM-1 levels (P = 0.005). The level of sPECAM-1 was further correlated to soluble platelet selectin (sP-selectin, also measured by ELISA), platelet count, and total white blood cell count (WBC), suggesting that platelets are a major source of sPECAM-1 and platelet activation and inflammation may contribute to PECAM-1 elevations in CAD patients. Conclusion: The Leu125Val polymorphism of PECAM-1 and the level of sPECAM-1 are associated with CAD in Chinese in Singapore. The level of sPECAM-1 is also associated with platelet activation and inflammation and correlated to the Leu125Val polymorphism. Our data suggest that PECAM-1 plays an important role in the development of atherosclerosis.

High plasma lipoprotein(a) [Lp(a)] level is a strong and important risk factor for cardiovascular disease (CVD). Small-sized apolipoprotein(a) [apo(a)] isoforms (F, B, S1, and S2) are inversely correlated with the high levels of Lp(a) in plasma and significantly associated with CVD. Although the effects of apo(a) phenotypes and various risk factors on Lp(a) status in South Asian population may have been studied in other countries, there are no reports involving these risk factors in Australia.Factors contributing to variation in Lp(a) were surveyed in 402 (216 males and 186 females) South Asian Melburnians. There was a negative relationship between low alcohol beer per day and Lp(a) in men (P0.05). Approximately 21% of the variance of Lp(a) concentration in men and 6% in women were explained by age. Age was positively associated with Lp(a) concentrations in men but negatively in women. The most commonly occurring phenotype was apo(a) S3. In this phenotype, Lp(a) concentrations ranged from non-detectable to 811 mg/l. After adjusting for age, an inverse correlation was observed between Lp(a) concentration and apo(a) phenotypes (P0.01).Although Lp(a) has been reported to be genetically determined, there are clearly other factors contributing to variations in Lp(a) concentrations in a South Asian population.

Background —Intracoronary γ- and β-radiation have reduced restenosis in animal models. In the clinical setting, the effectiveness of β-emitters has not been studied in a broad spectrum of patients, particularly those receiving stents. Methods and Results —A prospective, randomized, sham-controlled study of intracoronary radiotherapy with the β-emitting 32 P source wire, using a centering catheter and automated source delivery unit, was conducted. A total of 105 patients with de novo (70%) or restenotic (30%) lesions who were treated by stenting (61%) or balloon angioplasty (39%) received 0 (control), 16, 20, or 24 Gy to a depth of 1 mm in the artery wall. Angiography at 6 months showed a target site late loss index of 11±36% in radiotherapy patients versus 55±30% in controls ( P P =0.012) and at target site plus adjacent segments (22% versus 50%; P =0.018). Target lesion revascularization was needed in 5 radiotherapy patients (6%) and 6 controls (24%; P Conclusions —β-radiotherapy with a centered 32 P source is safe and highly effective in inhibiting restenosis at the target site after stent or balloon angioplasty. However, minimizing edge narrowing and late thrombotic events must be accomplished to maximize the clinical benefit of this modality.

The 5-month angiographic in-stent restenosis rate did not differ between patients with chronic total occlusions (n = 43) and subtotal stenoses (n = 43) equally matched for diabetes status, exact stent design, final expanded stent diameter, stent length, and residual percent diameter stenosis after stent placement; it was 32.5% and 27.9% for those with chronic total occlusions and subtotal stenoses, respectively (p = 0.638). Furthermore, the stent occlusion rate (4.6% vs 6.9%, respectively) was low in both patient groups.

just prior to rupture (57% of cases) and (ii) a prolonged hypotensive and bradycardiac period (possibly due to incomplete rupture), followed by rupture upon complete recoveryofBPandHR (43%). In conclusion, hemodynamic factors do seem to play a role in the pathogenesis of postinfarct rupture on the background of a severely weakened infracted myocardium. doi:10.1016/j.hlc.2008.05.565

Summary Although volumetric, haemodynamic and nutritional factors may be involved in causing the circulatory changes of pregnancy, steroid hormones are now favoured as prime movers of the train of events leading to a hyperkinetic circulation.

Summary The naturally occurring oestrogens, oestrone and oestriol, were given by intraarterial infusion into the brachial artery and by intravenous injection. No changes in blood flow through the hand or forearm were observed with either route of administration. Intravenous injection resulted in a significant rise in blood pressure but no significant changes in heart rate or limb vascular resistance. It is suggested that this rise in blood pressure may be due to a direct action of the hormones on the heart.

Hemodynamic changes were monitored serially in a group of 30 healthy young women receiving combined estrogen-progestogen oral contraceptive (OC) therapy. Significant increases in cardiac output (expressed as cardiac index) systolic and mean blood pressures and plasma volume occurred during therapy. Changes in heart rate and diastolic blood pressure were not significant. An increase in stroke volume was mainly responsible for the increase in cardiac output. Plasma renin substrate and renin activity increased renin concentration decreased while blood angiotensin levels increased markedly during OC administration in all 13 of 30 subjects in whom these investigations were carried out. A significant increase in body weight occurred in most subjects while receiving OC therapy. (authors)