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Lifestyle and Hemostatic Risk Factors for Ischemic Heart Disease : The Caerphilly Study
- John W. G. Yarnell,
- Peter M. Sweetnam,
- Ann Rumley and
- Gordon D. O. Lowe
Arteriosclerosis, Thrombosis, and Vascular Biology Volume 20, Issue 11 January 2000

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Abstract— We have recently shown that fibrin D-dimer, tissue plasminogen activator (tPA) antigen, von Willebrand factor antigen, fibrinogen, plasma viscosity, and white cell count are associated with subsequent ischemic heart disease (IHD) in men aged 49 to 65 years in the Caerphilly Study from South Wales. We now report the contribution of major lifestyle factors to plasma levels of these new risk predictors for IHD. Results were available for up to 2188 men. The contribution of factors associated with lifestyle (smoking, alcohol, body mass index, leisure and work activity, social class, and use of prescribed medicines) to variation in plasma levels of 8 hemostatic variables was examined. All results were adjusted for other lifestyle variables, age, and time of day. Most hemostatic variables increased with age and smoking habit. Increasing levels of alcohol consumption were associated with increases in tPA and plasminogen activator inhibitor (PAI-1) activity and with decreases in fibrinogen and white cell count. tPA, PAI-1, fibrinogen (nephelometric), and viscosity were positively associated with body mass index. Increasing levels of leisure activity were inversely associated with D-dimer, von Willebrand factor, nephelometric fibrinogen, and viscosity. Use of prescribed medicines (a marker for chronic illness) was associated with adverse levels of D-dimer, fibrinogen, plasma viscosity, and white cell count. tPA, PAI-1, and plasma viscosity were associated with blood pressure, cholesterol, and triglycerides but not with lipoprotein(a) or homocysteine. We conclude that several lifestyle factors are associated with hemostatic risk predictors for IHD. Lifestyle modifications may reduce IHD risk partly by altering hemostatic function; large intervention studies are required to test this hypothesis.
Adverse Neonatal and Cardiac Outcomes Are More Common in Pregnant Women With Cardiac Disease
- Samuel C. Siu,
- Jack M. Colman,
- Sheryll Sorensen,
- Jeffrey F. Smallhorn,
- Dan Farine,
- Kofi S. Amankwah,
- John C. Spears and
- Mathew Sermer
Circulation Volume 105, Issue 187 May 2002

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Background— Pregnant women with heart disease (HD) are at increased risk for cardiac (CV) complications. However, the frequency of neonatal (NE) complications in pregnant women with HD relative to pregnant women without HD has not been examined.Methods and Results— Pregnant women with HD were prospectively monitored during 302 pregnancies. The frequency of NE and CV complications was compared with those in a control group without HD during 572 pregnancies. The frequency of NE complications was higher in the HD group (18% versus 7%; HD versus controls). The NE complication rate was lowest in pregnancies of women age 20 to 35 years who did not smoke during pregnancy, did not receive anticoagulants, and had no obstetric risk factors: 4% in control patients, 5% in HD patients with no cardiac risk factors for NE complications (left heart obstruction, poor functional class, or cyanosis), and 7% in HD patients with ≥1 such risk factor. In contrast, the event rate in pregnancies of controls age <20 or >35 years who had obstetric risk factors or multiple gestation or who smoked was 11%. In the HD group, women age <20 or >35 years who had obstetric risk factors or multiple gestation, who smoked, or who received anticoagulants experienced an even higher NE complication rate (27% with no cardiac risks for NE events and 33% in the presence of ≥1 cardiac risk factors). The frequency of CV complications was higher in the HD group (17% versus 0%; HD versus controls).Conclusion— Pregnant women with HD are at increased risk for both NE and CV complications. The risk for NE adverse events in pregnant women with HD is highest in those with both obstetric and cardiac risk factors for NE complications.
Long-Term Use of Contraceptive Depot Medroxyprogesterone Acetate in Young Women Impairs Arterial Endothelial Function Assessed by Cardiovascular Magnetic Resonance
- Morten B. Sorensen,
- Peter Collins,
- Paul J.L. Ong,
- Carolyn M. Webb,
- Christopher S. Hayward,
- Elizabeth A. Asbury,
- Peter D. Gatehouse,
- Andrew G. Elkington,
- Guang Z. Yang,
- Ali Kubba and
- Dudley J. Pennell
Circulation Volume 106, Issue 1324 September 2002

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Background— Depot medroxyprogesterone acetate (DMPA) inhibits proliferation of ovarian follicles, resulting in anovulation and a decrease in circulating estrogen; the latter action is potentially disadvantageous to cardiovascular health. We therefore investigated the vascular effects of long-term contraceptive DMPA in young women.Methods and Results— Endothelium-dependent (hyperemia-induced flow-mediated dilatation [FMD]) and -independent (glyceryl trinitrate [GTN]) changes in brachial artery area were measured using cardiovascular magnetic resonance in 13 amenorrheic DMPA users (>1 year use; mean age 29±4 years) and in 10 controls (mean age 30±4 years, P=0.25) with regular menstrual cycles after validation of the technique. FMD and GTN responses were measured just before repeat MPA injection and 48 hours later (n=12) in DMPA users and during menstruation and midcycle (n=9) in controls. Serum-estradiol levels (S-estradiol) were measured at both visits. FMD was reduced in DMPA users compared with controls during menstruation (1.1% versus 8.0%, respectively P<0.01) without differences in GTN responses. S-estradiol levels in DMPA users were significantly lower than in controls during menstruation (58 versus 96 pmol/L, P<0.01). High levels of circulating MPA 48 hours after injection were not linked to an additional impairment in FMD (2.0% versus 3.1%, P=0.23). Estradiol levels were significantly correlated to FMD (r=0.43, P<0.01).Conclusions— Endothelium-dependent arterial function measured by cardiovascular magnetic resonance is impaired in chronic users of DMPA, and hypoestrogenism may be the mechanism of action. DMPA might adversely affect cardiovascular health, and in particular its use in women with cardiovascular disease should be additionally evaluated.
Visualization of Ventricular Thrombi With Contrast-Enhanced Magnetic Resonance Imaging in Patients With Ischemic Heart Disease
- Nico R. Mollet,
- Steven Dymarkowski,
- Wim Volders,
- Jurgen Wathiong,
- Lieven Herbots,
- Frank E. Rademakers and
- Jan Bogaert
Circulation Volume 106, Issue 233 December 2002

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Background— Ventricular thrombus formation is a frequent and potentially dangerous complication in patients with ischemic heart disease. Although transthoracic echocardiography (TTE) is generally used as diagnostic technique, we explored the role of contrast-enhanced (CE)-MRI to detect ventricular thrombi.Methods and Results— In 57 patients with acute myocardial infarction, chronic myocardial infarction, or ischemic cardiomyopathy, MRI was performed to evaluate ventricular function (CINE-MRI) and to depict presence of myocardial necrosis and/or scarring and no-reflow areas (CE-MRI). All studies were analyzed for concomitant ventricular thrombi. CE-MRI depicted 12 mural thrombi (3.1±2.9 cm³), located in left ventricular (LV) apex or adherent to anteroseptum, presenting as black, well-defined structures surrounded by bright contrast-enhanced blood. Thrombus formation on CE-MRI was related to larger end-diastolic volumes; lower ejection fractions; the region of delayed enhancement and lowest wall motion score, especially in left anterior descending coronary artery territory; and LV aneurysm formation. On CINE-MRI, thrombi were found in 6 patients. Nonvisualized thrombi were usually small (mean size 1.2±0.7 cm³). TTE depicted thrombi in 5. Nonvisualized lesions were most frequently located in LV apex and had a larger size than nonvisualized lesions on CINE-MRI (3.0±3.2 cm³). In 3 patients with suspected apical thrombus on TTE, MRI was normal.Conclusions— CE-MRI is not only an excellent technique to depict myocardial necrosis and scar tissue in patients with ischemic heart disease, but this study also suggests a better identification of LV thrombi than with presently used clinical imaging modalities, such as TTE.
The VIVA Trial: Vascular Endothelial Growth Factor in Ischemia for Vascular Angiogenesis
- Timothy D. Henry,
- Brian H. Annex,
- George R. McKendall,
- Michael A. Azrin,
- John J. Lopez,
- Frank J. Giordano,
- P.K. Shah,
- James T. Willerson,
- Raymond L. Benza,
- Daniel S. Berman,
- C. Michael Gibson,
- Alex Bajamonde,
- Amy Chen Rundle,
- Jennifer Fine,
- Edward R. McCluskey
Circulation Volume 107, Issue 1018 March 2003

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Background— Recombinant human vascular endothelial growth factor protein (rhVEGF) stimulates angiogenesis in animal models and was well tolerated in Phase I clinical trials. VIVA (Vascular endothelial growth factor in Ischemia for Vascular Angiogenesis) is a double-blind, placebo-controlled trial designed to evaluate the safety and efficacy of intracoronary and intravenous infusions of rhVEGF.Methods and Results— A total of 178 patients with stable exertional angina, unsuitable for standard revascularization, were randomized to receive placebo, low-dose rhVEGF (17 ng · kg⁻¹ · min⁻¹), or high-dose rhVEGF (50 ng · kg⁻¹ · min⁻¹) by intracoronary infusion on day 0, followed by intravenous infusions on days 3, 6, and 9. Exercise treadmill tests, angina class, and quality of life assessments were performed at baseline, day 60, and day 120. Myocardial perfusion imaging was performed at baseline and day 60. At day 60, the change in exercise treadmill test (ETT) time from baseline was not different between groups (placebo, +48 seconds; low dose, +30 seconds; high dose, +30 seconds). Angina class and quality of life were significantly improved within each group, with no difference between groups. By day 120, placebo-treated patients demonstrated reduced benefit in all three measures, with no significant difference compared with low-dose rhVEGF. In contrast, high-dose rhVEGF resulted in significant improvement in angina class (P=0.05) and nonsignificant trends in ETT time (P=0.15) and angina frequency (P=0.09) as compared with placebo.Conclusions— rhVEGF seems to be safe and well tolerated. rhVEGF offered no improvement beyond placebo in all measurements by day 60. By day 120, high-dose rhVEGF resulted in significant improvement in angina and favorable trends in ETT time and angina frequency.
Physical Activity in Relation to Cardiovascular Disease and Total Mortality Among Men With Type 2 Diabetes
- Mihaela Tanasescu,
- Michael F. Leitzmann,
- Eric B. Rimm and
- Frank B. Hu
Circulation Volume 107, Issue 1920 May 2003

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Background— The present study was conducted to examine the relationship of physical activity with risk of cardiovascular disease (CVD) and mortality among men with type 2 diabetes. CVD risk and mortality are increased in type 2 diabetes. Few epidemiological studies have investigated the effect of physical activity on these outcomes among type 2 diabetics.Methods and Results— Of the 3058 men who reported a diagnosis of diabetes at age 30 years or older in the Health Professionals’ Follow-up Study (HPFS), we excluded 255 who reported a physical impairment. In the remaining 2803 men, physical activity was assessed every 2 years; 266 new cases of CVD and 355 deaths of all causes were identified during 14 years of follow-up. Relative risks of CVD and death were estimated from Cox proportional hazards analysis with adjustment for potential confounders. The multivariate relative risks of CVD incidence corresponding to quintiles of total physical activity were 1.0, 0.87, 0.64, 0.72, and 0.67 (P_trend=0.07). The corresponding multivariate relative risks for total mortality were 1.0, 0.80, 0.57, 0.58, and 0.58 (P_trend=0.005). Walking was associated with reduced risk of total mortality. Relative risks across quintiles of walking were 1.0, 0.97, 0.87, 0.97, and 0.57 (P_trend=0.002). Walking pace was inversely associated with CVD, fatal CVD, and total mortality independently of walking hours.Conclusions— Physical activity was associated with reduced risk of CVD, cardiovascular death, and total mortality in men with type 2 diabetes. Walking and walking pace were associated with reduced total mortality.
Increased Thrombosis After Arterial Injury in Human C-Reactive Protein–Transgenic Mice
- Haim D. Danenberg,
- Alexander J. Szalai,
- Rajesh V. Swaminathan,
- Lin Peng,
- Zhiping Chen,
- Philip Seifert,
- William P. Fay,
- Daniel I. Simon and
- Elazer R. Edelman
Circulation Volume 108, Issue 55 August 2003

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Background— C-reactive protein (CRP), an acute-phase reactant long considered merely an innocent bystander in the inflammatory process, is now recognized as a powerful predictor of cardiovascular events. Emerging in vitro evidence suggests that CRP may have direct proinflammatory and prothrombotic effects on monocytes and endothelial cells. To determine whether CRP directly modulates vascular cell function in vivo, we subjected wild-type mice, which do not express CRP, and human CRP–transgenic (CRPtg) mice to 2 models of arterial injury.Methods and Results— Baseline serum CRP levels in CRPtg mice were 18±6 mg/L. CRP levels were undetectable in wild-type mice. Transluminal wire injury led to complete thrombotic occlusion of the femoral artery at 28 days in 75% of CRPtg arteries (6 of 8) compared with 17% (2 of 12) in wild-type mice (P<0.05). In a model of arterial photochemical injury, clot formation time was shortened in CRPtg mice; mean time to occlusion was 33±19 minutes compared with 59±19 minutes in wild-type mice (n=10; P<0.05).Conclusions— Arterial injury in CRPtg mice results in an expedited and higher rate of thrombotic occlusion. This is the first report of a prothrombotic phenotype directly attributable to the presence of human CRP in vivo. Investigation of the inflammatory-thrombotic axis in CRPtg mice may elucidate the prothrombotic actions of CRP in unstable arterial diseases and may pave the way for novel therapeutic interventions for preventing cardiovascular events.
Orthotopic Heart Transplantation for Congenital Heart Disease: An Alternative for High-Risk Fontan Candidates?
- Guido Michielon,
- Francesco Parisi,
- Cosimo Squitieri,
- Adriano Carotti,
- Giulia Gagliardi,
- Luciano Pasquini and
- Roberto M. Di Donato
Circulation Volume 108, Issue 10_suppl_19 September 2003

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Objective— Evaluation of incremental risk factors for early mortality in children undergoing orthotopic heart transplantation (OHT) for congenital heart disease.Methods— Between 1988 and 2002, 43 patients (mean age 9.1±7.2 years) underwent 44 OHT for complex TGA (6), DORV (4), single ventricle (21), and other end-stage structural heart disease (11). Two discernible ventricular chambers were present in 18 pts (41.8%). Previous reconstructive or palliative procedures had been previously accomplished in 35 pts (83.3%), including atrial switch (5), systemic-to-pulmonary shunts (10), cavopulmonary anastomosis (9), Fontan completion (6), and others (5).Results— 30-day survival for the 2-ventricle subgroup was 94.4±5.4% compared with 67.2±9.5% for the single ventricle subgroup (P=0.04) (overall 78.6%±3.3%). OHT following single ventricle staging to bi-directional cavopulmonary anastomosis exhibited 100% early survival, as opposed to 62.5±17.1% for OHT after systemic-to-pulmonary shunts, and 33.3±19.2% for OHT following failing Fontan (P=0.010). HLHS diagnosis (0.0085) and failing Fontan (P=0.003) were identified as independent predictors of early mortality by regression logistic modeling, while Fontan stage represented the only predictor of overall mortality by Cox proportional hazard. Overall 10-year survival was 54.3±11%.Conclusions— OHT for structural congenital heart disease with single ventricle physiology entails substantial early mortality and bi-directional cavopulmonary anastomosis enables the best transition to heart transplant. OHT should be considered in the decision making process as an alternative to Fontan completion in high-risk candidates, since rescue-OHT after failing Fontan seems unwarranted.
Regulated on Activation, Normal T Cell Expressed and Secreted (RANTES) Antagonist (Met-RANTES) Controls the Early Phase of Trypanosoma cruzi–Elicited Myocarditis
Circulation Volume 110, Issue 1114 September 2004

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Background— Comprehension of the pathogenesis of Trypanosoma cruzi–elicited myocarditis is crucial to delineate strategies aimed at ameliorating the inflammation associated with heart dysfunction. The augmented expression of CC chemokines, especially CCL5/RANTES and CCL3/MIP-1α, in the hearts of infected mice suggests a role for CC chemokines and their receptors in the pathogenesis of T cruzi–elicited myocarditis.Methods and Results— We report that during the early phase of infection in C3H/HeJ mice infected with 100 blood trypomastigotes of T cruzi, most of the inflammatory cells invading the heart tissue were CD8⁺ cells and expressed CCR5, a CCL5/RANTES, and CCL3/MIP1-α receptor. Furthermore, peripheral blood CD8⁺ T lymphocytes displayed increased expression of CCR5. These findings led us to use Met-RANTES, a selective CCR1 and CCR5 antagonist, to modulate the acute T cruzi–elicited myocarditis. Met-RANTES treatment did not interfere with parasitism but significantly decreased the numbers of CD4⁺ and CD8⁺ T cells, CCR5⁺, and interleukin-4⁺ cells invading the heart, paralleling the diminished deposition of fibronectin. Moreover, Met-RANTES treatment resulted in increased survival of infected animals, compared with saline treatment.Conclusions— These results indicate that the massive influx of CCR5⁺ cells into cardiac tissue is not crucial for cell-mediated anti–T cruzi immunity but appears to be critical for pathogenesis of T cruzi–elicited myocarditis. Thus, CC chemokine receptors might become an attractive therapeutic target for further evaluation during T cruzi infection.
Opposing Effects of C-Reactive Protein Isoforms on Shear-Induced Neutrophil-Platelet Adhesion and Neutrophil Aggregation in Whole Blood
- Tarek Khreiss,
- Levente József,
- Lawrence A. Potempa and
- János G. Filep
Circulation Volume 110, Issue 1726 October 2004

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Background— Plasma C-reactive protein (CRP) level is a powerful predictor of cardiovascular events. However, it is not known whether CRP could affect neutrophil-platelet adhesion and neutrophil aggregation, key events in acute coronary syndromes. Emerging in vitro evidence suggests that some bioactivities of CRP are expressed on loss of the pentameric symmetry, resulting in formation of modified or monomeric CRP (mCRP).Methods and Results— We studied the impact of human native CRP and bioengineered mCRP that cannot rearrange into the pentameric structure on the kinetics of neutrophil-platelet adhesion and neutrophil aggregation in whole blood subjected to shear (≈100 s⁻¹) using real-time flow cytometry. Shear resulted in upregulation of platelet P-selectin expression, leading to platelet capture of neutrophils and subsequent neutrophil aggregation, which was dependent on P-selectin, L-selectin, and CD18. Native CRP at clinically relevant concentrations markedly attenuated these changes. The residual amount of neutrophil adhesion was blocked with anti-CD18 or anti-CD11b antibody. By contrast, mCRP concentration-dependently enhanced shear-induced platelet P-selectin expression and increased the rate and extent of formation of both neutrophil-platelet and neutrophil-neutrophil aggregates. Complete abrogation of platelet-neutrophil adhesion and neutrophil aggregation required both anti-P-selectin and anti-CD18 antibodies but not anti-L-selectin antibody. The CRP action was markedly inhibited by an anti-CD32 antibody, whereas the mCRP effects were significantly attenuated by an anti-CD16 antibody.Conclusions— These results indicate that native CRP inhibits platelet activation and prevents platelet capture of neutrophils, whereas mCRP displays potent prothrombotic activities under low levels of shear. Thus, mCRP rather than native CRP may precipitate acute coronary syndromes.
Linear Cryoablation of the Left Atrium Versus Pulmonary Vein Cryoisolation in Patients With Permanent Atrial Fibrillation and Valvular Heart Disease: Correlation of Electroanatomic Mapping and Long-Term Clinical Results
- Fiorenzo Gaita,
- Riccardo Riccardi,
- Domenico Caponi,
- Dipen Shah,
- Lucia Garberoglio,
- Laura Vivalda,
- Alessandro Dulio,
- Andrea Chiecchio,
- Eric Manasse and
- Roberto Gallotti
Circulation Volume 111, Issue 218 January 2005

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Background— The aim of this study was to clarify the role of pulmonary vein isolation (PVI) alone versus left atrial linear lesions in the treatment of permanent atrial fibrillation (AF) in patients with left atrial dilatation and valvular disease. The primary end point was to assess the persistence of sinus rhythm (SR) off antiarrhythmic drugs (AADs) at 2-year follow-up and to correlate clinical outcome with surgical results validated with electroanatomic mapping (EAM).Methods and Results— A total of 105 patients with permanent AF undergoing valve surgery were assigned to 3 different groups: in groups “U” and “7,” left atrial linear cryoablation was performed, whereas in group “PV” patients, anatomic cryoisolation of pulmonary veins only was performed. In groups U and 7, SR was achieved in 57% of patients, whereas it was achieved in 20% of PV patients during 2-year follow-up. In the first 51 patients, the ablation schemes were validated with EAM. The EAM showed that the U lesion was never obtained: in 59% of these patients, a complete 7 lesion was achieved instead; in the 7 group, a complete 7 lesion was present in 65% of patients, whereas a complete PVI was obtained in 71% of patients. Considering patients in whom a complete 7 lesion was demonstrated with the EAM, SR without AADs was achieved in 86% of patients, whereas only 25% of patients with complete PVI were in SR without AADs.Conclusions— In patients with permanent AF, left atrial dilatation and valvular heart disease linear lesions in the posterior region of the left atrium are more effective than PVI alone. With cryoablation, the surgical intent is fulfilled in only approximately 65% of the cases. Knowing the real anatomic and electrophysiological effects of surgical ablation is necessary to correctly interpret the clinical outcome.
Relationships Between Homocysteine, Factor VIIa, and Thrombin Generation in Acute Coronary Syndromes
- Mohamed K. Al-Obaidi,
- Helen Philippou,
- Peter J. Stubbs,
- Antonella Adami,
- Rajiv Amersey,
- Mark M. Noble and
- David A. Lane
Circulation Volume 101, Issue 41 February 2000

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Background—It has been suggested by clinical, epidemiological, and experimental in vitro studies that homocysteine potentiates thrombin generation. This prothrombotic effect however has not previously been demonstrated in patients presenting with acute coronary syndromes (ACS).Methods and Results—Patients with ACS (n =117) presenting with confirmed acute myocardial infarction (MI) (n =57) or unstable angina pectoris (UAP) (n =60) were consecutively recruited together with patients (n =18) in whom the presenting chest pain was not of cardiac origin (NCP), included as controls. Plasma samples were collected on admission and before clinical intervention. Homocysteine was assayed by high performance liquid chromatography, and both Factor VIIa and prothrombin fragment F1+2 were analyzed by ELISA. There were significant elevations in F1+2 in MI (P<0.001) and UAP (P=0.003), and modest elevations in Factor VIIa in UAP (P<0.05) compared with NCP but no differences in homocysteine levels among those groups. On dividing patients with ACS into quartiles of homocysteine, there was a stepwise increase in F1+2 (P<0.0001) and of Factor VIIa (P<0.05). There were significant correlations in ACS between homocysteine and F1+2 (r=0.46, P<0.0001), homocysteine and Factor VIIa (r=0.24, P<0.01), and F1+2 and Factor VIIa (r=0.41, P<0.0001). There was no correlation between homocysteine and either F1+2 (r=−0.15, P=0.57) or Factor VIIa (r=0.22, P=0.37) in the NCP patients.Conclusions—Elevated plasma homocysteine is associated with and may cause elevated Factor VIIa and thrombin generation in patients presenting with ACS. These findings suggest an explanation for the prothrombotic effect of homocysteine in ACS.
AHA Dietary Guidelines : Revision 2000: A Statement for Healthcare Professionals From the Nutrition Committee of the American Heart Association
- Ronald M. Krauss,
- Robert H. Eckel,
- Barbara Howard,
- Lawrence J. Appel,
- Stephen R. Daniels,
- Richard J. Deckelbaum,
- John W. Erdman,
- Penny Kris-Etherton,
- Ira J. Goldberg,
- Theodore A. Kotchen,
- Alice H. Lichtenstein,
- William E. Mitch,
- Rebecca Mullis,
- Killian Robinson,
- Judith Wylie-Rosett,
- Sachiko St. Jeor,
- John Suttie,
- Diane L. Tribble and
- Terry L. Bazzarre
Circulation Volume 102, Issue 1831 October 2000

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Isolated Mitral Valve Replacement With St Jude Medical Prosthesis : Long-Term Results: A Follow-Up of 19 Years
- J. P. Remadi,
- O. Baron,
- C. Roussel,
- P. Bizouarn,
- Al Habasch,
- P. Despins,
- J. L. Michaud and
- D. Duveau
Circulation Volume 103, Issue 1120 March 2001

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Background—In this retrospective study, ≈440 patients received mitral valve replacements with the St Jude Medical prothesis. The last patient was operated on 10 years before the beginning of the follow-up. The extended follow-up was 19 years.Methods and Results—Four hundred forty patients (sex ratio, 1.32 [men to women]; age, 60±11.4 years; age range, 7 to 75 years) were operated on from 1979 to 1987. All patients underwent isolated mitral valve replacement. Tricuspid plasty was the only associated procedure. The follow-up at 19 years was 98% complete. The overall actuarial survival rate was 63±3.3% at 19 years, and the actuarial survival rate (only valve related) was 83±2.7%. The operative mortality rate (0 to 30 days) was 4.09%. We found that 89.4% of the patients alive at 19 years were in NYHA class I/II. Multivariate analysis showed that age and sex were significantly correlated with valve-related mortality and that age, sex, NYHA class, and atrial fibrillation were significantly correlated with overall mortality. The linearized rates (percent patient-years) of thromboembolism, thrombosis, and hemorrhage were 0.69, 0.2, and 1, respectively. At 19 years, freedom from endocarditis and reoperation was 98.6±1% and 90±3%, respectively.Conclusions—In this study, the very-long-term results confirm the excellent durability of the St Jude Medical prosthesis in the mitral position and show the difficulty of adjusting the anticoagulation protocol, even after long-term treatment.
Increased Particulate Air Pollution and the Triggering of Myocardial Infarction
- Annette Peters,
- Douglas W. Dockery,
- James E. Muller and
- Murray A. Mittleman
Circulation Volume 103, Issue 2312 June 2001

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Background—Elevated concentrations of ambient particulate air pollution have been associated with increased hospital admissions for cardiovascular disease. Whether high concentrations of ambient particles can trigger the onset of acute myocardial infarction (MI), however, remains unknown.Methods and Results—We interviewed 772 patients with MI in the greater Boston area between January 1995 and May 1996 as part of the Determinants of Myocardial Infarction Onset Study. Hourly concentrations of particle mass <2.5 μm (PM_2.5), carbon black, and gaseous air pollutants were measured. A case-crossover approach was used to analyze the data for evidence of triggering. The risk of MI onset increased in association with elevated concentrations of fine particles in the previous 2-hour period. In addition, a delayed response associated with 24-hour average exposure 1 day before the onset of symptoms was observed. Multivariate analyses considering both time windows jointly revealed an estimated odds ratio of 1.48 associated with an increase of 25 μg/m³ PM_2.5 during a 2-hour period before the onset and an odds ratio of 1.69 for an increase of 20 μg/m³ PM_2.5 in the 24-hour period 1 day before the onset (95% CIs 1.09, 2.02 and 1.13, 2.34, respectively).Conclusions—The present study suggests that elevated concentrations of fine particles in the air may transiently elevate the risk of MIs within a few hours and 1 day after exposure. Further studies in other locations are needed to clarify the importance of this potentially preventable trigger of MI.
Angiogenesis Therapy : Amidst the Hype, the Neglected Potential for Serious Side Effects
- Stephen E. Epstein,
- Ran Kornowski,
- Shmuel Fuchs and
- Harold F. Dvorak
Circulation Volume 104, Issue 13 July 2001

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Carcinoid Heart Disease
- Allen S. Anderson,
- Daniel Krauss,
- Claudia Korcarz and
- Roberto M. Lang
Circulation Volume 93, Issue 11 January 1996

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Air Travel and Adults With Cyanotic Congenital Heart Disease
- Eric Harinck,
- Paul A. Hutter,
- Theo M. Hoorntje,
- Marinus Simons,
- Avram A. Benatar,
- Johan C. Fischer,
- Dagmar de Bruijn and
- Erik Jan Meijboom
Circulation Volume 93, Issue 215 January 1996

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Background Concern has been expressed that a reduction of partial oxygen pressure during flight in commercial aircraft may induce dangerous hypoxemia in patients with cyanotic congenital heart disease. Methods and Results To evaluate the validity of this concern, the transcutaneous Sao₂ was measured in 12 adults with this type of heart disease and 27 control subjects during simulated commercial flights of 1.5 and 7 hours in a hypobaric chamber. Ten of those patients and 6 control subjects also were evaluated during two actual flights of approximately 2.5 hours in a DC-10 and an A-310, respectively. During the prolonged simulated and actual flights, the capillary blood pH, gases, and lactic acid were analyzed in the patients and during one of the actual flights also in the control subjects. During the simulated flights the Sao₂ was at all times lower in the patients than in the control subjects. However, the maximal mean actual percentage decrease, as compared with sea level values, did not exceed 8.8% in either patients or control subjects. During the actual flights, this maximal decrease in the patients was 6%. In-flight reduction of the capillary Po₂ was considerable in the control subjects but not in the patients. It is our hypothesis that the lack of a significant decrease of the Po₂ in the patients might possibly be due to a high concentration of 2.3 diphosphoglycerate in the red cells. The flights had no influence on the capillary blood pH, Pco₂, bicarbonate, or lactic acid levels in either patients or control subjects. Conclusions Atmospheric pressure changes during commercial air travel do not appear to be detrimental to patients with cyanotic congenital heart disease.
Ventricular Tachycardia in Valvular Heart Disease : Facilitation of Sustained Bundle-Branch Reentry by Valve Surgery
- Calambur Narasimhan,
- Mohammad R. Jazayeri,
- Jasbir Sra,
- Anwer Dhala,
- Sanjay Deshpande,
- Michael Biehl,
- Masood Akhtar and
- Zalmen Blanck
Circulation Volume 96, Issue 1216 December 1997

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Background The clinical characteristics of sustained monomorphic ventricular tachycardia (SMVT), when it develops after valve surgery, have not been described.Methods and Results Between 1985 and 1996, 31 patients (30 men and 1 woman) who had undergone valve surgery were found to have inducible SMVT. Nine patients (29%) had sustained VT due to bundle-branch reentry (BBR) (group 1). Four of these patients had normal left ventricular function, and VT with a right bundle-branch morphology was inducible in 4 patients. Group 2 included 20 patients with inducible myocardial (ie, non-BBR) VT. Coronary artery disease was present in 15 group 2 patients (75%) due to atherosclerotic (n=12) and nonatherosclerotic (n=3) causes. Two patients had both inducible sustained BBR and myocardial VT (group 3). Sustained BBR VT occurred significantly earlier after valve surgery (median, 10 days) than the onset of postoperative myocardial VT (median, 72 months; P<.005).Conclusions Myocardial VT was the most common type of inducible SMVT in patients with valvular heart disease. The majority of these patients had underlying coronary artery disease and significant left ventricular dysfunction. However, in almost one third of the patients, sustained BBR VT was the only type of inducible SMVT. This type of VT was facilitated by the valve procedure occurring within 4 weeks after surgery in most patients. In these patients, left ventricular function was relatively well preserved, and the right bundle-branch block type of BBR was frequently induced. Because a curative therapy can be offered to these patients (ie, bundle-branch ablation), BBR should be seriously considered as the mechanism of VT in patients with valvular heart disease, particularly if the arrhythmia occurs soon after valve surgery.
Preventing Coronary Heart Disease : B Vitamins and Homocysteine
Circulation Volume 97, Issue 510 February 1998

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