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Research ArticleExamples of Clinical Research Programs at Ochsner

Preventive Cardiology and Non-Invasive Cardiology Research at the Ochsner Clinic Foundation

Carl J. Lavie, Richard V. Milani, Yvonne Gilliland, J. Alberto Bernal, Homeyar Dinshaw and Hector O. Ventura
Ochsner Journal March 2006, 6 (1) 31-35;
Carl J. Lavie
Ochsner Heart & Vascular Institute, Department of Cardiology, Ochsner Clinic Foundation
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Richard V. Milani
Ochsner Heart & Vascular Institute, Department of Cardiology, Ochsner Clinic Foundation
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Yvonne Gilliland
Ochsner Heart & Vascular Institute, Department of Cardiology, Ochsner Clinic Foundation
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J. Alberto Bernal
Ochsner Heart & Vascular Institute, Department of Cardiology, Ochsner Clinic Foundation
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Homeyar Dinshaw
Ochsner Heart & Vascular Institute, Department of Cardiology, Ochsner Clinic Foundation
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Hector O. Ventura
Ochsner Heart & Vascular Institute, Department of Cardiology, Ochsner Clinic Foundation
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Cardiovascular diseases (CVD), including coronary heart disease (CHD), stroke, and heart failure (HF) remain the leading cause of morbidity and mortality in all of western civilization and certainly this is the case in southern Louisiana. In this manuscript, we briefly review some of the preventive cardiology and non-invasive research performed at the Ochsner Heart and Vascular Institute in New Orleans, particularly data from our cardiac rehabilitation and exercise training (CRET) programs, clinical data from our cardiopulmonary laboratory regarding heart failure (HF) prognosis, as well as retrospective data from our cardiovascular informations systems (CVIS), which has allowed us to link a large volume of non-invasive data with subsequent prognosis.

BENEFITS OF CRET

During the past 15 years our institution has contributed significantly to the body of literature available regarding potential benefits of CRET (Table) to improve exercise capacity and overall levels of fitness (which is, in fact, one of the most potent predictors of overall CVD prognosis) in various subgroups of patients (including elderly and women); obesity indices; metabolic syndrome (MS); diabetes mellitus (DM); and plasma lipids (1–24), as well as numerous benefits in the areas of psychological factors (depression, anxiety, and hostility) and overall health-related quality of life (25–33). We have also demonstrated the benefits of this therapy to reduce the risk factor highly-sensitive Creactive protein (HSCRP) (24,34,35), a marker of inflammation, to improve autonomic function (a risk factor for CVD and especially sudden cardiac death or SCD) (36,37), to improve indices of ventricular repolarization dispersion (a marker of increased risk of malignant ventricular dysrhythmias and SCD) (38,39), as well as to reduce levels of homocysteine (associated with increased risk of CHD and stroke) (40) and improve blood rheology (reductions in blood viscosity and improvements in oxygen transport to tissues) (41).

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Table - Benefits of Cardiac Rehabilitation and Exercise Training Programs

To further highlight a few of these major findings, we studied 235 consecutive CHD patients following major CHD events who entered and completed CRET and compared them with 42 control CHD patients (following coronary events who did not attend formal CRET) (24). As expected, our CHD patients had moderately elevated levels of HSCRP at baseline (above 3 mg/l), and these levels fell by nearly 40% following CRET (Figure 1). Since statins have been demonstrated to significantly reduce HSCRP, it was important that we also demonstrated that the fall in HSCRP was independent of statin use, occurring equally in the majority of patients treated with statins as well as in those not treated with statins. Since adipocytes or fat cells synthesize cytokines involved in the production of HSCRP, and obesity is known to be associated with high levels of HSCRP which improve with weight loss, it was also important that we demonstrated that the fall in HSCRP following CRET was also independent of weight loss, occurring equally in our patients who lost weight as well as those few who actually gained weight during rehabilitation. We have also demonstrated that our patients with MS have significantly higher levels of HSCRP compared with CHD patients without MS (22,23), and the levels of HSCRP rose proportionately to the number of metabolic factors that are present, reaching very high levels in patients with three – five positive metabolic factors (Figure 2).

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Figure 1: Median changes in HSCRP in cardiac rehabilitation and in control CHD patients.24

Figure 2.
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Figure 2.

Relation between number of metabolic risk factors comprising MS and levels of hs-CRP before and after cardiac rehabilitation and exercise training.22

In addition, we believe that behavioral factors and psychological factors have often been under-appreciated as risk factors for CVD and these factors (depression, anxiety, and hostility) are also associated with worse prognosis in patients with CVD (25–33). We have demonstrated a high prevalence of psychological dysfunction in our patients with CHD, with particularly high levels of anxiety and hostility in our younger CHD patients (both older and younger patients have an approximately 20% prevalence of symptoms of depression). All of these adverse psychological factors improve markedly following formal CRET programs, along with the marked improvements that occurred in the rest of the CHD risk profiles in these patients with high levels of psychological distress.

HEART FAILURE (HF) RESEARCH

Our HF / cardiomyopathy group has been extremely prolific in the investigation of patients with HF and cardiac transplantation, and the non-invasive laboratories from OCF have also contributed to these areas of research.

One of the major ways to evaluate patients with severe systolic HF who are being considered for cardiac transplantation is cardiopulmonary exercise testing which provides precise determination of peak oxygen consumption or peak V02 (42–44). Generally, most major HF programs as well as most cardiopulmonary stress testing laboratories correct the peak V02 for total body weight as opposed to lean body mass, although body fat does not utilize substantial aerobic metabolism or perfusion. Several years ago we demonstrated that correcting peak V02 to lean body mass (determined by assessing percent body fat by a number of methods; we use the very simple sum of the skinfold method) performed considerably better than uncorrected peak V02 for predicting cardiac death and need for urgent cardiac transplantation (Figure 3) (45). More recently, we demonstrated that oxygen pulse (peak V02 / peak heart rate, which is a non-invasive marker of stroke volume as well as incorporating the arteriovenous oxygen difference) also performed better than peak V02, more so when correcting for lean body mass (Figure 4) (46).

Figure 3.
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Figure 3.

Kaplan-Meier survival curves using both PkVO2 of 14 ml/kg/min and PkVO2 lean of 19 ml/kg/min as cutoffs showing a stronger prognostic value to the fat-adjusted PkVO2 by log-rank testing. PkVO2 = peak oxygen consumption; PkVO2 lean = peak oxygen consumption adjusted to lean body mass; VO2 = oxygen consumption.45

Figure 4.
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Figure 4.

Kaplan-Meier survival curves using both peak O2– pulse 10 ml/beat and peak O2 – pulse lean 14 ml/beat as cut-offs for predicting event-free survival.46

There has also been considerable controversy regarding the role of obesity and pathogenesis of HF as well as HF prognosis (47, 48). Although clearly obesity has adverse effects on cardiac structure and function, and predisposes to the development of HF, we recently demonstrated a paradox regarding obesity and body composition parameters and HF prognosis (47–49). In fact, among our patients with severe systolic HF, those with the highest body mass indices and those with the highest percent body fat had the best prognosis (Figure 5) (49). In multivariate analysis, a higher percent body fat was the strongest independent predictor of event – free survival. In fact, for every 1% increase in percentage body fat, there was a nearly 15% reduction in major CVD events in these patients with severe systolic HF. We believe that these data support the concept of an “obesity paradox” which has also now been demonstrated by others. The reasons for this apparent obesity paradox are uncertain. However, studies have suggested that the natriuretic peptide system and adiposity are closely linked; our group has recently demonstrated reduced natriuretic peptide levels in obese patients with HF (47,50). This lends credence to the explanation that the earlier expression of HF in the presence of obesity could be related to reduced circulating natriuretic peptides. Therefore, obese HF patients may present earlier due to symptoms at a less severe level of HF, therefore promoting discordance between symptoms and prognosis. As we discussed above, it is recognized that peak oxygen consumption with exercise is a potent predictor or prognosis in advance HF and for practical purposes, fat does not consume oxygen or receive substantial perfusion. As we demonstrated above that lean adjusted exercise indices all predict prognosis better than non-fat adjusted variables, this may be particularly applicable to the favorable prognosis in HF patients with a high percentage body fat who generally have relatively high lean-adjusted exercise indices (47,49). In addition, most of the major HF studies, including our own, have not accounted for the effects of purposeful weight loss, which may be associated with more advanced HF and a poor prognosis. Clearly, purposeful weight loss in HF patients with morbid obesity has been associated with improvements in systolic and diastolic function and HF classification, but no large studies have determined the impact that purposeful weight reduction has on HF prognosis and mortality in either patients with preserved or abnormal systolic function (47–49). Finally, other lines of evidence have suggested enhanced protection with obesity against endotoxin/inflammatory cytokines as well as increased nutritional and metabolic reserve (47,50). Certainly, obesity could be associated with a better prognosis in HF and this relationship is not necessarily causal.

Figure 5.
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Figure 5.

Summary of body composition quintiles comparing major clinical events (cardiovascular death and urgent transplantation) during an average of 19 months of follow-up in the first quintile versus the fifth quintile for BMI, percent body fat (% Fat), and total fat in the total cohort (n=209).49

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Carl J. Lavie, MD, Ochsner Heart & Vascular Institute, Department of Cardiology, Ochsner Clinic Foundation

We have also utilized echocardiography to predict allograft rejection in patients following heart transplantation (51) and demonstrated the benefits of statins to reduce allograft rejection and improve survival in these transplant patients (52).

CVIS RESEARCH

Using a robust databank that now includes nearly 75,000 echocardiographic studies of patients who have often been followed for 3–5 years, we have studied the impact of left ventricular geometry (concentric remodeling and eccentric and concentric left ventricular hypertrophy) on survival (53–57) as well as indices of transmural dispersion of repolarization (a marker of increased risk of ventricular dysrhythmias) (58). In addition, we have assessed the prevalence of left ventricular diastolic dysfunction in patients with normal systolic function and the effects on survival (both isolated diastolic dysfunction as well as combined diastolic dysfunction and abnormalities in left ventricular geometry) (59,60). We have also assessed the prevalence of elevated pulmonary artery pressures in patients with structurally normal hearts and the impact of obesity on these increased pulmonary pressures (60,61). We have assessed the impact of valvular regurgitation particularly combined with elevated pulmonary artery systolic pressures on subsequent survival (63), and most recently we have studied a relatively new concept (left ventricular strain and ventricular elastance) in hypertensives and transplant patients, as well as in patients with various left ventricular geometric patterns (64,65). We anticipate that a huge quantity of these data will be published from our non-invasive laboratories in the next several years as this research is ongoing and continuing in the post-Katrina era.

CONCLUSIONS

Although trends indicate that CVD and CHD have been declining during recent decades, these same statistics also tell us that with the aging of our population, the absolute prevalence of CVD is still increasing and the cost of CVD, even adjusted for inflation, is also increasing. Therefore, the prevention and treatment of CVD will continue to be a major emphasis for many years to come. It is hoped that the continued research from these areas at Ochsner Clinic Foundation will at least partly contribute to the prevention and treatment of CVD both locally and at a national level.

  • Ochsner Clinic and Alton Ochsner Medical Foundation

REFERENCES

  1. ↵
    1. Lavie C. J.,
    2. Milani R. V.,
    3. Littman A. B.
    (1993) Benefits of cardiac rehabilitation and exercise training in secondary coronary prevention in the elderly. J Am Coll Cardiol 22:678–683, pmid:8354798.
    OpenUrlFREE Full Text
    1. Lavie C. J.,
    2. Milani R. V.
    (1993) Factors predicting improvements in lipid values following cardiac rehabilitation and exercise training. Arch Intern Med 153:982–988, pmid:8481069.
    OpenUrlCrossRefPubMed
    1. Lavie C. J.,
    2. Milani R. V.,
    3. Cassidy M. M.,
    4. Gilliland Y. E.
    (1995) Benefits of cardiac rehabilitation and exercise training in older persons. Am J Geriatr Cardiol 4:42–48, pmid:11416343.
    OpenUrlPubMed
    1. Lavie C. J.,
    2. Milani R. V.
    (1994) Patients with high baseline exercise capacity benefit from cardiac rehabilitation and exercise training programs. Am Heart J 128(6, part 1):1105–1109, pmid:7985590.
    OpenUrlCrossRefPubMed
    1. Lavie C. J.,
    2. Milani R. V.
    (1996) Effects of cardiac rehabilitation and exercise training in obese patients with coronary artery disease. Chest 109:52–56, pmid:8549217.
    OpenUrlCrossRefPubMed
    1. Lavie C. J.,
    2. Milani R. V.
    (1994) Effects of cardiac rehabilitation and exercise training on low-density lipoprotein cholesterol in patients with hypertriglyceridemia and coronary artery disease. Am J Cardiol 74:1192–1195, pmid:7977088.
    OpenUrlCrossRefPubMed
    1. Lavie C. J.,
    2. Milani R. V.
    (1995) Effects of cardiac rehabilitation and exercise training on exercise capacity, coronary risk factors, behavioral characteristics, and quality of life in women. Am J Cardiol 75:340–343, pmid:7856524.
    OpenUrlCrossRefPubMed
    1. Lavie C. J.,
    2. Milani R. V.
    (1995) Effects of cardiac rehabilitation programs on exercise capacity, coronary risk factors, behavioral characteristics, and quality of life in a large elderly cohort. Am J Cardiol 76:177–179, pmid:7611156.
    OpenUrlCrossRefPubMed
    1. Lavie C. J.,
    2. Milani R. V.,
    3. Ventura H. O.,
    4. Messerli F. H.,
    5. Murgo J. P.
    (1995) Cardiac rehabilitation, exercise training, and preventive cardiology research at Ochsner Heart and Vascular Institute. Tex Heart Inst J 22:44–52, pmid:7787470.
    OpenUrlPubMed
    1. Milani R. V.,
    2. Lavie C. J.
    (1995) Prevalence and effects of nonpharmacologic treatment of “isolated” low-HDL cholesterol in patients with coronary artery disease. J Cardiopulm Rehabil 15:439–444, pmid:8624971.
    OpenUrlPubMed
    1. Maines T. Y.,
    2. Lavie C. J.,
    3. Milani R. V.
    (1997) Effects of cardiac rehabilita-tion and exercise programs on exercise capacity, coronary risk factors, behavior, and quality of life in patients with coronary artery disease. South Med J 90:43–49, pmid:9003823.
    OpenUrlPubMed
    1. Lavie C. J.,
    2. Milani R. V.
    (1996) Effects of cardiac rehabilitation programs in patients ≥75 years of age. Am J Cardiol 78:675–677, pmid:8831404.
    OpenUrlCrossRefPubMed
    1. Lavie C. J.,
    2. Milani R. V.
    (1997) Benefits of cardiac rehabilitation and exercise training in elderly women. Am J Cardiol 79:664–666, pmid:9068528.
    OpenUrlCrossRefPubMed
    1. Lavie C. J.,
    2. Milani R. V.
    (1996) Effects of nonpharmacologic therapy with cardiac rehabilitation and exercise training in patients with low levels of high-density lipoprotein cholesterol. Am J Cardiol 78:1286–1289, pmid:8960593.
    OpenUrlCrossRefPubMed
    1. Lavie C. J.,
    2. Milani R. V.
    (1997) Effects of cardiac rehabilitation, exercise training, and weight reduction on exercise capacity, coronary risk factors, behavioral characteristics and quality of life in obese coronary patients. Am J Cardiol 79:397–401, pmid:9052338.
    OpenUrlCrossRefPubMed
    1. Milani R. V.,
    2. Lavie C. J.
    (1998) The effects of body composition changes to observed improvements in cardiopulmonary parameters after exercise training with cardiac rehabilitation. Chest 113:599–601, pmid:9515831.
    OpenUrlCrossRefPubMed
    1. Milani R. V.,
    2. Lavie C. J.
    (1998) Disparate effects of outpatient cardiac and pulmonary rehabilitation programs on work efficiency and peak aerobic capacity in patients with coronary disease or severe obstructive pulmonary disease. J Cardiopulm Rehabil 18:17–22, pmid:9494878.
    OpenUrlCrossRefPubMed
    1. Lavie C. J.,
    2. Milani R. V.
    (1999) Effects of cardiac rehabilitation and exercise training on peak aerobic capacity and work efficiency in obese patients with coronary artery disease. Am J Cardiol 83:1477–1480, pmid:10335765.
    OpenUrlCrossRefPubMed
    1. Lavie C. J.,
    2. Milani R. V.,
    3. Cassidy M. M.,
    4. Gilliland Y. E.,
    5. Bernal J. A.
    (1999) Cardiopulmonary rehabilitation, exercise training, and preventive cardiology - an overview of a decade of research at the Ochsner Heart and Vascular Institute. The Ochsner Journal 1:177–186, pmid:21845136.
    OpenUrlAbstract/FREE Full Text
    1. Lavie C. J.,
    2. Milani R. V.
    (2000) Disparate effects of improving exercise capacity and quality of life after cardiac rehabilitation in young and elderly coronary patients. J Cardiopulm Rehabil 20:235–40, pmid:10955264.
    OpenUrlCrossRefPubMed
    1. Lavie C. J.,
    2. Milani R. V.
    (2001) Benefits of cardiac rehabilitation and exercise training programs in elderly coronary patients. Am J Geriatr Cardiol 10:323–327, pmid:11684916.
    OpenUrlCrossRefPubMed
  2. ↵
    1. Milani R. V.,
    2. Lavie C. J.
    (2003) Prevalence and profile of metabolic syndrome in patients following acute coronary events and effects of therapeutic lifestyle change with cardiac rehabilitation. Am J Cardiol 92:50–54, pmid:12842245.
    OpenUrlPubMed
  3. ↵
    1. Lavie C. J.,
    2. Milani R. V.
    (2005) Cardiac rehabilitation and exercise training programs in metabolic syndrome and diabetes. J Cardiopulm Rehabil 25:59–66, pmid:15818190.
    OpenUrlPubMed
  4. ↵
    1. Milani R. V.,
    2. Lavie C. J.,
    3. Mehra M. R.
    (2004) Reduction in Creactive protein through cardiac rehabilitation and exercise training. J Am Coll Cardiol 43:1056–1061, pmid:15028366.
    OpenUrlFREE Full Text
  5. ↵
    1. Milani R. V.,
    2. Lavie C. J.,
    3. Cassidy M. M.
    (1996) Effects of cardiac rehabilitation and exercise training programs on depression in patients after major coronary events. Am Heart J 132:726–732, pmid:8831359.
    OpenUrlCrossRefPubMed
    1. Milani R. V.,
    2. Lavie C. J.
    (1996) Behavioral differences and effects of cardiac rehabilitation in diabetic patients following cardiac events. Am J Med 100:517–523, pmid:8644763.
    OpenUrlCrossRefPubMed
    1. Lavie C. J.,
    2. Milani R. V.
    (1999) Effects of cardiac rehabilitation and exercise training programs on coronary patients with high levels of hostility. Mayo Clin Proc 74:959–966, pmid:10918860.
    OpenUrlCrossRefPubMed
    1. Milani R. V.,
    2. Lavie C. J.
    (1998) Prevalence and effects of cardiac rehabilitation on depression in the elderly with coronary artery disease. Am J Cardiol 81:1233–1236, pmid:9604957.
    OpenUrlCrossRefPubMed
    1. Lavie C. J.,
    2. Milani R. V.,
    3. Cassidy M. M.,
    4. Gilliland Y. E.
    (1999) Benefits of cardiac rehabilitation and exercise training programs in women with depression. Am J Cardiol 83:1480–1483, pmid:10335766.
    OpenUrlCrossRefPubMed
    1. Lavie C. J.,
    2. Milani R. V.
    (2004) Prevalence of anxiety in coronary patients with improvement following cardiac rehabilitation and exercise training. Am J Cardiol 93:336–339, pmid:14759385.
    OpenUrlCrossRefPubMed
    1. Lavie C. J.,
    2. Milani R. V.
    (2004) Impact of aging on hostility in coronary patients and effects of cardiac rehabilitation and exercise training in the elderly. Am J Geriatr Cardiol 13:125–130, pmid:15133415.
    OpenUrlPubMed
    1. Lavie C. J.,
    2. Milani R. V.
    (2005) Prevalence of hostility in young coronary patients and effects of cardiac rehabilitation and exercise training. Mayo Clin Proc 80:335–342, pmid:15757014.
    OpenUrlCrossRefPubMed
    1. Lavie C. J.,
    2. Milani R. V.
    (2004) Adverse psychological and coronary risk profiles in young patients and benefits of formal cardiac rehabilitation. Circulation 110(17):792, suppl III.
    OpenUrl
  6. ↵
    1. Milani R. V.,
    2. Lavie C. J.
    (2004) Does inflammation influence cardiovascular risk factor modification. Circulation 109:e29, pmid:14769691.
    OpenUrlFREE Full Text
  7. ↵
    1. Lavie C. J.,
    2. Milani R. V.
    (2004) Metabolic syndrome, inflammation, and exercise. Am J Cardiol 93:1334, pmid:15135724.
    OpenUrlPubMed
  8. ↵
    1. Lucini D.,
    2. Milani R. V.,
    3. Costantino G.,
    4. Lavie C. J.,
    5. Porta A.,
    6. Pagani M.
    (2002) Effects of cardiac rehabilitation and exercise training on autonomic regulation in patients with coronary artery disease. Am Heart J 143:977–83, pmid:12075252.
    OpenUrlCrossRefPubMed
  9. ↵
    1. Lavie C. J.,
    2. Milani R. V.
    (2002) Autonomic tone and benefits of cardiac rehabilitation programs. Mayo Clin Proc 77:398–399, pmid:11936939.
    OpenUrlCrossRefPubMed
    1. Ali A.,
    2. Mehra M.,
    3. Malik F. S.,
    4. Lavie C. J.,
    5. Bass D.,
    6. Milani R. V.
    (1999) Effects of aerobic exercise training on indices of ventricular repolarization in patients with chronic heart failure. Chest 116:83–87, pmid:10424508.
    OpenUrlCrossRefPubMed
    1. Kalapura T.,
    2. Lavie C. J.,
    3. Jaffrani W.,
    4. Chilakamarri V.,
    5. Milani R. V.
    (2003) Effects of cardiac rehabilitation and exercise training on indexes of dispersion of ventricular repolarization in patients after acute myocardial infarction. Am J Cardiol 92:292–294, pmid:12888135.
    OpenUrlCrossRefPubMed
  10. ↵
    1. Arshad A.,
    2. Milani R. V.,
    3. Lavie C. J.,
    4. Malik F. S.,
    5. Murgo J. P.,
    6. Shuguang L.,
    7. Hun-Chi L.,
    8. Lohmann T. P.
    (1998) Modulatory impact of cardiac rehabilitation on hyperhomocysteinemia in patients with coronary artery disease and “normal” lipid levels. Am J Cardiol 82:1543–1545, pmid:9874065.
    OpenUrlCrossRefPubMed
  11. ↵
    1. Church T. S.,
    2. Lavie C. J.,
    3. Kirby G. S.,
    4. Milani R. V.
    (2002) Improvements in blood rheology after cardiac rehabilitation and exercise training in patients with coronary heart disease. Am Heart J 143:349–355, pmid:11835042.
    OpenUrlCrossRefPubMed
  12. ↵
    1. Milani R. V.,
    2. Mehra M. R.,
    3. Lavie C. J.
    (1996) Ventilation/carbon dioxide production ratio in early exercise predicts poor functional capacity and prognosis in congestive heart failure. Heart 76:393–396, pmid:8944583.
    OpenUrlAbstract/FREE Full Text
    1. Richards D. R.,
    2. Mehra M. R.,
    3. Ventura H. O.,
    4. Lavie C. J.,
    5. Smart F. W.,
    6. Stapleton D. D.,
    7. Milani R. V.
    (1997) Usefulness of peak oxygen consumption in predicting outcome of heart failure in women versus men. Am J Cardiol 80:1236–1238, pmid:9359563.
    OpenUrlCrossRefPubMed
    1. Milani R. V.,
    2. Lavie C. J.,
    3. Mehra M. R.
    (2004) Cardiopulmonary exercise testing: How do we differentiate the cause of dyspnea? Circulation 110:e27–e31, pmid:15277333.
    OpenUrlFREE Full Text
  13. ↵
    1. Osman A.,
    2. Lavie C. J.,
    3. Mehra M.,
    4. Milani R. V.
    (2000) The incremental prognostic importance of body fat adjusted peak oxygen consumption in chronic heart failure. J Am Coll Cardiol 36:2126–2131, pmid:11127451.
    OpenUrlFREE Full Text
  14. ↵
    1. Lavie C. J.,
    2. Milani R. V.,
    3. Mehra M. R.
    (2004) Peak exercise oxygen pulse and prognosis in chronic heart failure. Am J Cardiol 93:588–593, pmid:14996584.
    OpenUrlCrossRefPubMed
  15. ↵
    1. Lavie C. J.,
    2. Mehra M. R.,
    3. Milani R. V.
    (2005) Obesity and heart failure prognosis – Paradox or reverse epidemiology? Eur Heart J 26:5–7, pmid:15615792.
    OpenUrlCrossRefPubMed
  16. ↵
    1. Lavie C. J.,
    2. Milani R. V.
    (2003) Editorial Comment. Obesity and cardiovascular disease: The Hippocrates paradox? J Am Coll Cardiol 42:677–679, pmid:12932600.
    OpenUrlFREE Full Text
  17. ↵
    1. Lavie C. J.,
    2. Osman A. F.,
    3. Milani R. V.,
    4. Mehra M. R.
    (2003) Body composition and prognosis in chronic systolic heart failure: The obesity paradox. Am J Cardiol 91:891–894, pmid:12667583.
    OpenUrlCrossRefPubMed
  18. ↵
    1. Mehra M. R.,
    2. Uber P. A.,
    3. Park M. H.,
    4. Scott R. L.,
    5. Ventura H. O.,
    6. Harris B. C.,
    7. Frohlich E. D.
    (2004) Obesity and supporessed B-type natriuretic peptide levels in heart failure. J Am Coll Cardiol 43:1590–1595, pmid:15120816.
    OpenUrlFREE Full Text
  19. ↵
    1. Vivekananthan K.,
    2. Kalapura T.,
    3. Mehra M. R.,
    4. Lavie C. J.,
    5. Milani R. V.,
    6. Scott R. L.,
    7. Park M. H.
    (2002) Usefulness of the combined index of systolic and diastolic myocardial performance to identify cardiac allograft rejection. Am J Cardiol 90:517–520, pmid:12208413.
    OpenUrlCrossRefPubMed
  20. ↵
    1. Mehra M. R.,
    2. Uber P. A.,
    3. Vivekananthan K.,
    4. Solis S.,
    5. Scott R. L.,
    6. Park M. H.,
    7. Milani R. V.,
    8. Lavie C. J.
    (2002) Comparative beneficial effects of simvastatin and pravastatin on cardiac allograft rejection and survival. J Am Coll Cardiol 40:1609–1614, pmid:12427413.
    OpenUrlFREE Full Text
  21. ↵
    1. Milani R. V.,
    2. Lavie C. J.,
    3. Mehra M. R.,
    4. Ventura H. O.,
    5. Kurtz J.,
    6. Messerli F. H.
    Left ventricular geometry and survival in patients with preserved left ventricular ejection fraction. Am J Cardiol, in press.
    1. Lavie C. J.,
    2. Milani R. V.,
    3. Gilliland Y. E.,
    4. Bernal J. A.,
    5. Dinshaw H. K.,
    6. Ventura H. O.,
    7. Messerli F. H.
    (2004) Left ventricular geometry predicts mortality in elderly with preserved systolic function – An echocardiographic study in 9,771 patients over 70 years. Circulation 110:472, pmid:15289386, suppl III.
    OpenUrlFREE Full Text
    1. Lavie C. J.,
    2. Milani R. V.,
    3. Ventura H. O.,
    4. Morshedi-Meibodi A.
    (2004) Left ventricular mass versus relative wall thickness for predicting mortality in patients with preserved systolic function – An echocardiographic study in 35,607 patients. Circulation 110:516, suppl III.
    OpenUrl
    1. Cardenas G. A.,
    2. Milani R. V.,
    3. Lavie C. J.,
    4. Gilliland Y. E.
    (2005) Left ventricular geometry predicts mortality in women with preserved systolic function – an echocardiographic study in 17,851 patients. Circulation 111:e50.
    OpenUrl
    1. Morshedi-Meibodi A.,
    2. Ndandu Z.,
    3. Lavie C. J.,
    4. Milani R. V.,
    5. Messerli F. H.,
    6. Ventura H. O.
    (2003) Change in left ventricular mass index predicts all cause mortality. Circulation 108:449, suppl IV.
    OpenUrl
  22. ↵
    1. Saba M. M.,
    2. Arain S. A.,
    3. Lavie C. J.,
    4. Abi-Samra F. M.,
    5. Ibrahim S. S.,
    6. Ventura H. O.,
    7. Milani R. V.
    (2005) Relation between left ventricular geometry and transmural dispersion of repolarization. Am J Cardiol 96:952–955, pmid:16188523.
    OpenUrlCrossRefPubMed
  23. ↵
    1. Milani R. V.,
    2. Lavie C. J.,
    3. Mehra M. R.,
    4. Kurtz J.,
    5. Ventura H. O.
    (2003) Diastolic dysfunction: An important predictor of survival in patients with preserved systolic function. J Am Coll Cardiol 41:148A, suppl 1.
    OpenUrl
  24. ↵
    1. Milani R. V.,
    2. Mehra M. R.,
    3. Lavie C. J.,
    4. Ventura H. O.
    (2004) Combined effects of diastolic dysfunction and LV remodeling on mortality in 7,267 patients with preserved LV systolic function. J Am Coll Cardiol 43:241A, pmid:14736444, suppl 1.
    OpenUrlPubMed
  25. ↵
    1. Milani R. V.,
    2. Lavie C. J.,
    3. Rubiano A.
    (2002) Clinical correlates and reference intervals for pulmonary artery systolic pressure among echocardiographically normal subjects. Circulation 106:e19, pmid:12147552.
    OpenUrlFREE Full Text
    1. Milani R. V.,
    2. Lavie C. J.,
    3. Gilliland Y. E.,
    4. Vivekananthan K.,
    5. Cassidy M. M.,
    6. Bernal A. J.,
    7. Morshedi A.
    (2003) Pulmonary artery systolic pressure in echocardiographically normal subjects. J Am Coll Cardiol 41:257A, suppl 1.
    OpenUrl
  26. ↵
    1. Milani R. V.,
    2. Lavie C. J.,
    3. Gilliland Y. E.,
    4. Cassidy M. M.,
    5. Bernal J. A.,
    6. Mulumudi M.
    (2003) Effect of pulmonary artery systolic pressure on mortality in patients with mitral regurgitation and normal systolic function. J Am Coll Cardiol 41:511A, suppl 2.
    OpenUrl
  27. ↵
    1. Milani R. V.,
    2. Mehra M. R.,
    3. Lavie C. J.,
    4. Ventura H. O.
    (2003) Evidence for increased cardiac and peripheral arterial vascular stiffening in heart transplantation independent of hypertension. Circulation 108:545, suppl IV.
    OpenUrl
  28. ↵
    1. Milani R. V.,
    2. Lavie C. J.,
    3. Ventura H. O.
    (2004) Combined ventricular systolic and arterial stiffening in patients with concentric remodeling and preserved systolic function. Circulation 110:678, suppl III.
    OpenUrl
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Preventive Cardiology and Non-Invasive Cardiology Research at the Ochsner Clinic Foundation
Carl J. Lavie, Richard V. Milani, Yvonne Gilliland, J. Alberto Bernal, Homeyar Dinshaw, Hector O. Ventura
Ochsner Journal Mar 2006, 6 (1) 31-35;

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Preventive Cardiology and Non-Invasive Cardiology Research at the Ochsner Clinic Foundation
Carl J. Lavie, Richard V. Milani, Yvonne Gilliland, J. Alberto Bernal, Homeyar Dinshaw, Hector O. Ventura
Ochsner Journal Mar 2006, 6 (1) 31-35;
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