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William Chan,
Dion Stub,
David J Clark,
Andrew E Ajani,
Nick Andrianopoulos,
Angela L Brennan,
Gishel New,
Alexander Black, James A Shaw,
Christopher M Reid,
Anthony M Dart,
Stephen J Duffy
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ABSTRACT: The no reflow phenomenon is reported to occur in >2% of all percutaneous coronary interventions (PCIs) and portends a poor prognosis. We analyzed data from 5,286 consecutive patients who underwent PCI from the Melbourne Interventional Group (MIG) registry from April 2004 through January 2008 who had 30-day follow-up completed. Patients without no reflow (normal reflow, n = 5,031) were compared to 255 (4.8%) with no reflow (n = 217 for transient no reflow, n = 38 for persistent no reflow). Patients with transient or persistent no reflow were more likely to present with ST-elevation myocardial infarction (MI) or cardiogenic shock (p <0.0001 for the 2 comparisons). They were also more likely to have complex lesions (American College of Cardiology/American Heart Association type B2/C), have lesions within a bypass graft, require an intra-aortic balloon pump, receive glycoprotein IIb/IIIa inhibition, and have a longer mean stent length (p <0.0001 for all comparisons). In-hospital outcomes were significantly worse in those patients with transient or persistent no reflow, with increased death, periprocedural MI, renal impairment, and major adverse cardiac events (p <0.0001 for all comparisons). Similarly, transient and persistent no reflow portended worse 30-day clinical outcomes, with a progressive increase in mortality (normal reflow 1.7% vs transient no reflow 5.5% vs persistent no reflow 13.2%, p <0.0001), MI, target vessel revascularization, and major adverse cardiac events (p <0.0001 for all comparisons) compared to patients with normal flow. In conclusion, transient or persistent no reflow complicates approximately 1 in 20 PCIs and results in stepwise increases in in-hospital and 30-day adverse outcomes.
The American journal of cardiology 12/2011; 109(4):478-85. · 3.58 Impact Factor
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Dion Stub,
Christopher Hengel,
William Chan,
Damon Jackson,
Karen Sanders,
Anthony M Dart,
Andrew Hilton,
Vincent Pellegrino, James A Shaw,
Stephen J Duffy,
Stephen Bernard,
David M Kaye
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ABSTRACT: Survival rates after out-of-hospital cardiac arrest (OHCA) continue to be poor. Recent evidence suggests that a more aggressive approach to postresuscitation care, in particular combining therapeutic hypothermia with early coronary intervention, can improve prognosis. We performed a single-center review of 125 patients who were resuscitated from OHCA in 2 distinct treatment periods, from 2002 to 2003 (control group) and from 2007 to 2009 (contemporary group). Patients in the contemporary group had a higher prevalence of cardiovascular risk factors but similar cardiac arrest duration and prehospital treatment (adrenaline administration and direct cardioversion). Rates of cardiogenic shock (48% vs 41%, p = 0.2) and decreased conscious state on arrival (77% vs 86%, p = 0.2) were similar in the 2 cohorts, as was the incidence of ST-elevation myocardial infarction (33% vs 43%, p = 0.1). The contemporary cohort was more likely to receive therapeutic hypothermia (75% vs 0%, p <0.01), coronary angiography (77% vs 45%, p <0.01), and percutaneous coronary intervention (38% vs 23%, p = 0.03). This contemporary therapeutic strategy was associated with better survival to discharge (64% vs 39%, p <0.01) and improved neurologic recovery (57% vs 29%, p <0.01) and was the only independent predictor of survival (odds ratio 5.5, 95% confidence interval 1.2 to 26.2, p = 0.03). Longer resuscitation time, presence of cardiogenic shock, and decreased conscious state were independent predictors of poor outcomes. In conclusion, modern management of OHCA, including therapeutic hypothermia and early coronary angiography is associated with significant improvement in survival to hospital discharge and neurologic recovery.
The American journal of cardiology 02/2011; 107(4):522-7. · 3.58 Impact Factor
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Michelle J Butler,
David Eccleston,
David J Clark,
Andrew E Ajani,
Nick Andrianopoulos,
Angela Brennan,
Gishel New,
Alexander Black,
Gregory Szto,
Chris M Reid,
Bryan P Yan, James A Shaw,
Anthony M Dart,
Stephen J Duffy
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ABSTRACT: The optimal duration of clopidogrel use for prevention of stent thrombosis with drug-eluting stent (DES) use is uncertain. Our objective was to determine whether the planned duration of clopidogrel at the time of percutaneous coronary intervention affected patient outcomes.
We analyzed data from 2,980 patients who underwent percutaneous coronary intervention in the Melbourne Interventional Group registry who had 12-month follow-up. We compared outcomes at 30 days and 12 months according to planned duration of clopidogrel use.
Twelve-month mortality was significantly lower in patients with a DES with a longer (>or=12 months) planned duration of clopidogrel when compared with a shorter (<or=6 months) planned duration (2.8% vs 5.3%, P = .012). However, myocardial infarction, target-vessel revascularization, and overall major adverse cardiac events were similar in the longer- and shorter-duration clopidogrel strategies. In contrast, in patients receiving a bare-metal stent, mortality at 12 months was similar among the clopidogrel-duration strategies. Kaplan-Meier analysis demonstrated improved cumulative survival with planned clopidogrel use of >or=12 months (log rank P = .017), and the propensity score-adjusted odds ratio was 0.59 (95% confidence interval 0.35-0.99, P = .04). Premature cessation of clopidogrel in DES patients was documented in 5.2% of patients alive at 30-day follow-up, and these patients had increased 12-month mortality (10.6% vs 1.4%, P < .0001) and major adverse cardiac events (22.4% vs 12.0%, P = .005).
These data suggest that in patients treated with DES, longer (>or=12 months) planned duration of clopidogrel results in reduced 12-month mortality and that premature cessation of clopidogrel results in significantly higher event rates. Randomized studies are urgently needed to address this issue.
American heart journal 05/2009; 157(5):899-907. · 4.65 Impact Factor
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ABSTRACT: Inflammation and structural factors such as a thin fibrous cap, positive remodeling and large lipid pool have been established as factors associated with coronary plaque instability. This study aimed to investigate the hypothesis that the differential in coronary artery compliance between stenotic and adjacent arterial segments is another factor associated with unstable coronary disease.
Forty-one patients undergoing a percutaneous coronary intervention were classified as unstable coronary syndrome (n=19) or stable angina (n=22). Intravascular ultrasound was used to assess external elastic lamina (EEL) cross-sectional area at diastole and systole. Aortic pressure was determined from the coronary guiding catheter. Coronary cross-sectional compliance (C) was calculated as the quotient of systolic-to-diastolic area differential and pulse pressure. C was measured within the stenosis and the adjacent reference segments.
EEL cross-sectional area was greater in systole than in diastole in the reference segments, but did not differ within the lesion site. C was greater in the distal reference than the stenotic segments (7.7+/-13.1 vs. 0.0+/-12.3mm(2)mmHg(-1)x10(3), p=0.003). When dichotomized by clinical presentation, the distal-to-stenosis compliance difference was only significant in the unstable coronary syndrome group (stable: distal 4.1+/-13.3 vs. stenosis -0.3+/-13.2mm(2)mmHg(-1)x10(3), ANOVA p=0.48; unstable: distal 11.9+/-11.9 vs. stenosis 0.1+/-11.6mm(2)mmHg(-1)x10(3), ANOVA p=0.006, distal-to-stenosis difference p=0.001).
A difference between stenotic and distal reference segment coronary compliance was evident in unstable, but not stable coronary artery disease patients. Coronary compliance differential would increase cyclical forces in the plaque shoulder region, which may contribute to plaque disruption.
Atherosclerosis 04/2009; 206(1):179-85. · 3.79 Impact Factor
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ABSTRACT: Studies have shown a reduction in plaque volume and change in plaque ultrasound characteristics after 4 infusions of reconstituted high-density lipoprotein (rHDL). Whether rHDL infusion leads to acute changes in plaque characteristics in humans is not known. Patients with claudication scheduled for percutaneous superficial femoral artery revascularization were randomized to receive 1 intravenous infusion of either placebo or rHDL (80 mg/kg given over 4 hours). Five to 7 days following the infusion, patients returned and revascularization was performed including atherectomy to excise plaque from the superficial femoral artery. Twenty patients (17 males) average age, 68+/-10 years (mean+/-SD) were recruited. Eleven patients had a history of documented coronary artery disease, all patients were on aspirin, and 18 were on statins. Ten of the patients received rHDL and 10 placebo. There was significantly less vascular cell adhesion molecule-1 expression (28+/-3% versus 50+/-3%; P<0.05) and a reduction in lipid content in the plaque of HDL-treated subjects compared to placebo. The level of HDL cholesterol increased by 20% after infusion of rHDL and the capacity of apolipoprotein B-depleted plasma to support cholesterol efflux increased. Intravenous infusion of a single dose of reconstituted HDL led to acute changes in plaque characteristics with a reduction in lipid content, macrophage size, and measures of inflammation. These changes may contribute to the cardioprotective effects of HDL.
Circulation Research 10/2008; 103(10):1084-91. · 9.49 Impact Factor
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Andrew E Ajani,
Christopher M Reid,
Stephen J Duffy,
Nick Andrianopoulos,
Jeffrey Lefkovits,
Alexander Black,
Gishel New,
Robert Lew, James A Shaw,
Bryan P Yan,
Ronen Gurvitch,
Ali Al-Fiadh,
Angela L Brennan,
David J Clark
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ABSTRACT: To examine short- and medium-term outcomes of percutaneous coronary interventions (PCIs), with a focus on comparing drug-eluting stents (DESs) with bare-metal stents (BMSs).
Retrospective analysis of data from the Melbourne Interventional Group (MIG) registry, a large multicentre Australian registry. The study cohort consisted of 6364 consecutive patients undergoing 7167 PCIs between April 2004 and August 2007.
Clinical events including death, myocardial infarction (MI), target lesion revascularisation (TLR), target vessel revascularisation (TVR) and major adverse cardiac events (MACE) (a composite of death, MI and TVR), at 30 days and at 12 months.
The cohort was predominantly male (74%), with a mean age of 64.7 years (SD, 12.0 years). DESs were used in 3482 (51.4%) of PCIs. In the overall cohort, rates of clinical events were low at 30 days: mortality (1.9%), MI (2.4%), TLR (2.0%), TVR (2.4%) and MACE (5.7%). At 12 months, event rates were: mortality (5.2%), MI (6.0%), TLR (5.8%), TVR (8.2%) and MACE (16.2%). Patients receiving DESs had similar mortality rates to those receiving BMSs (4.0% v 6.0%; P = 0.62 [propensity score-adjusted]); late thrombosis rates were also similar in the two groups (0.8% v 1.1%; P = 0.38). The proportion of patients receiving DESs fell significantly over time, from 54.9% in the first 24 months to 44.7% in the last 15 months of the study period (P < 0.01). Independent predictors of 12-month mortality included diabetes, renal failure, ST-segment-elevation MI and cardiogenic shock.
Our clinical event rates were comparable with international registry outcomes. Rates of mortality and stent thrombosis were no higher in patients with DESs than those with BMSs. Although DESs were used in about half the procedures (preferentially for higher-risk lesions), recent trends suggest their use is in decline.
The Medical journal of Australia 10/2008; 189(8):423-8. · 2.81 Impact Factor
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ABSTRACT: Matrix metalloproteinases (MMPs) are plausible candidates for prediction of unstable coronary syndromes. We hypothesised that the MMP-3 polymorphism (- 1171, 5A/6A) would relate to coronary plaque characteristics and unstable clinical presentation.
Forty patients with de novo presentation of coronary artery disease (CAD) were classified into unstable coronary syndrome (n=19) or stable angina pectoris (n=21). On coronary intravascular ultrasound, patients with unstable disease had a greater plaque burden, more positive (outward) coronary remodelling, and all but one were MMP-3 6A allele carriers (p=0.027 compared with stable). The relationship between the 6A allele and unstable presentation was substantiated in a validation cohort of 161 CAD patients (58 stable and 103 unstable) and in the total population of 201 CAD patients (79 stable and 122 unstable, p=0.007), and was independent of conventional risk factors. Furthermore, 6A allele carriers had a higher plasma MMP-3 concentration (15.8+/-12.5 versus 11.7+/-7.2 ng/mL, p=0.01), maximum coronary stenosis on angiography (89+/-15% versus 80+/-23%, p=0.02), plaque area (12.0+/-5.2 versus 7.5+/-3.6 mm(2), p=0.03), percentage plaque burden (82+/-7 versus 71+/-13%, p=0.003), and remodelling ratio (1.03+/-0.23 versus 0.83+/-0.12, p=0.003).
The MMP-3 6A allele promotes positive coronary remodelling, greater plaque burden, and increased susceptibility to unstable coronary syndromes in humans.
Cardiovascular Research 10/2007; 75(4):813-20. · 6.06 Impact Factor
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Arteriosclerosis Thrombosis and Vascular Biology 01/2007; 26(12):2826-7. · 6.37 Impact Factor
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ABSTRACT: Stent implantation in the rabbit aorta has been shown to increase vessel wall compliance at the inflow to the stent, but it is uncertain whether similar effects might be seen in the coronary arteries of humans and whether this would have any significant clinical consequences. First, we measured vessel compliance (systolic lumen area--diastolic lumen area/pulse pressure) before, immediately after, and at the 6-month follow-up visit at a site 5 mm upstream of the proximal edge of an implanted coronary stent in patients undergoing coronary intervention using motorized pull-back intravascular ultrasound recordings. Compliance in the upstream segment increased significantly immediately after stenting (before 7.13 +/- 1.49 vs after 10.73 +/- 1.36 mm2/mm Hg, p = 0.03), an effect that was unchanged at 6 months of follow-up (11.84 +/- 2.11 mm2/mm Hg, p = 0.08 vs before stenting). Second, we examined the site of plaque rupture in all patients presenting with an acute coronary syndrome in whom the culprit lesion was in a vessel that had had a stent implanted >12 months previously (n = 31). Plaque rupture was statistically more likely at the inflow to the stent (n = 22) than at other sites within the culprit vessel (n = 9, p <0.01). We conclude that stenting causes an increase in vessel compliance immediately proximal to the stent, and that when a vessel has been previously stented, plaque rupture is most likely to occur at the stent inflow site.
The American Journal of Cardiology 09/2005; 96(5):673-5. · 3.37 Impact Factor
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ABSTRACT: The goal of this study was to determine factors contributing to the biomechanical properties of coronary arteries in people with and without angiographic coronary artery disease (CAD).
The stiffness of the aorta is known to increase with increasing age and in the presence of CAD. However, little is known about the mechanics of coronary arteries, which may have important clinical consequences.
Intravascular ultrasound was used to determine the mechanical properties of coronary arteries and plaque behavior in subjects with CAD (n = 38), those with chest pain but angiographically normal coronary arteries (N) (n = 9) and those early (<2 weeks) after cardiac transplant (T) (n = 14).
Coronary arteries dilated during systole in all groups, but cross-sectional compliance and distensibility were lowest in the proximal left anterior descending artery (LAD) in the subjects with CAD compared with the N and T groups (compliance: 1.2 +/- 0.2 vs. 1.7 +/- 0.5 and 2.7 +/- 0.6 x 10(-2) mm(2) mm Hg(-1) [mean +/- SEM] respectively, p < 0.02 CAD vs. T; distensibility: 0.8 +/- 0.2 vs. 1.7 +/- 0.5 and 1.7 +/- 0.3 x 10(-3) mm Hg(-1), p < 0.05 CAD vs. T). There was extensive plaque in the CAD group, and plaque was also present in the N group, but minimal atheroma was present in the T group. Plaque cross-sectional area diminished significantly during systole in both the LAD and circumflex arteries. Absolute changes were: 0.50 +/- 0.30, 0.33 +/- 0.11 and 0.68 +/- 0.13 mm(2) in the proximal LAD, distal LAD and proximal circumflex arteries, respectively. In subjects with atheroma, there was a significant correlation between cross-sectional compliance and plaque compression at all sites, and plaque compression was a significant determinant of cross-sectional compliance at both proximal sites in multiple regression analyses with age, mean arterial pressure and extent of plaque as the other independent variables.
A major determinant of the systolic increase in coronary luminal area in patients with atheroma is a reduction in plaque cross-sectional area during systole.
Journal of the American College of Cardiology 05/2002; 39(10):1637-43. · 14.16 Impact Factor
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James A Shaw,
Nick Andrianopoulos,
Stephen Duffy,
Anthony S Walton,
David Clark,
Robert Lew,
Martin Sebastian,
Gishel New,
Angela Brennan,
Chris Reid,
Andrew E Ajani
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ABSTRACT: Renal impairment (RI) is known to be an independent risk factor for the progression of cardiovascular disease. Its impact, however, on the outcomes in patients undergoing percutaneous coronary intervention (PCI) especially in the era of drug-eluting stents (DES) is not well known. We analysed data from patients undergoing PCI from April 1, 2004, to September 30, 2006, who were part of the Melbourne Interventional Group registry. RI was defined as an estimated glomerular filtration rate (eGFR), calculated using Cockcroft-Gault formula, of <60 ml/min. We compared outcomes at 30 days and 12 months in patients with and without RI. Four thousand one hundred ninety-five patients (3043 male) with an average age 65+/-12 years (mean+/-S.D.) underwent PCI. Twelve-month follow-up was available in 3963 (95%) patients, and these were included in the analysis. One thousand twelve patients (26%) had RI; of these, 608 (60%) presented with an acute coronary syndrome. Both 30-day major adverse cardiac events (MACE), 9.1% vs. 4.6% (P<.01), and all-cause mortality, 4.5% vs. 0.7% (P<.01), were significantly higher in those with RI compared to those without RI. Twelve-month mortality (8.8% vs. 1.7%, P<.01) and MACE (19.7% vs. 10.3%, P<.01) were also significantly higher in those with RI. In multiple regression analysis, RI was an independent predictor of 12-month MACE [OR 2.0 (CI 1.6-2.6), P<.01]. RI is an independent predictor of 30-day and 12-month MACE and death after PCI in patients with stable and unstable coronary syndromes, even with widespread use of DES. eGFR should be used to help risk-stratify patients undergoing PCI.
Cardiovascular revascularization medicine: including molecular interventions 9(4):218-23.
