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Dive into the research topics where Hugh F. McIntyre is active.

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Featured researches published by Hugh F. McIntyre.


European Journal of Heart Failure | 2008

Mode of death in patients with newly diagnosed heart failure in the general population.

Paresh A Mehta; Simon W Dubrey; Hugh F. McIntyre; David Walker; Suzanna M C Hardman; George C. Sutton; Theresa McDonagh; Martin R. Cowie

Early prognosis for incident (new) heart failure (HF) patients in the general population is poor. Clinical trials suggest approximately half of chronic HF patients die suddenly but mode of death for incident HF cases in the general population has not been evaluated.


European Journal of Heart Failure | 2007

A high prevalence of sleep disordered breathing in men with mild symptomatic chronic heart failure due to left ventricular systolic dysfunction

Ali Vazir; Peter C. Hastings; M. Dayer; Hugh F. McIntyre; Michael Y. Henein; P.A. Poole-Wilson; Martin R. Cowie; Mary J. Morrell

Sleep disordered breathing (SDB) is common in severe chronic heart failure (CHF) and is associated with increased morbidity and mortality. The prevalence of SDB in mild symptomatic CHF is unknown.


International Journal of Cardiology | 2010

Adaptive servo-ventilation in heart failure patients with sleep apnea: A real world study

Peter C. Hastings; Ali Vazir; Guy E. Meadows; Mark Dayer; Philip A. Poole-Wilson; Hugh F. McIntyre; Mary J. Morrell; Martin R. Cowie

BACKGROUND Congestive heart failure (CHF) patients often present with obstructive and central sleep apnea occurring concurrently within the same night. This study assessed the efficacy of, and improvements associated with, the use of adaptive servo-ventilation (ASV) in CHF patients with all types of sleep apnea. We hypothesized that ASV would be effective at reducing sleep apnea and improving both cardiac status and quality of life. METHODS Eleven male patients with stable CHF and sleep apnea (apnea/hypopnea index (AHI) >15 events/h) were treated with 6 months optimized ASV and compared to 8 patients not receiving ASV. At baseline, both groups were comparable for New York Heart Association class, left ventricular ejection fraction (LVEF), plasma Brain Natriuretric Peptide (BNP) concentrations and AHI. All patients were receiving optimal medical therapy. RESULTS At 6 months ASV significantly reduced AHI (mean (SD), baseline 49.0 (35.1) v ASV 7.6 (14.6); p=0.001) and LVEF was increased (median (inter-quartile range), treatment group: +5.7 (1.6-9.5) v comparison group: -4.0 (-8.9-+4.6)% respectively; p=0.04) but not BNP (p=0.59). The energy/vitality score of the SF-36 quality of life questionnaire was also improved at 6 months (treatment group: +10 (5-35) v comparison group: -12 (-18-+10); p=0.005). CONCLUSION ASV effectively reduces all types of sleep apnea. Six months of use is associated with improvement in LVEF and aspects of quality of life.


Heart | 2009

Improving survival in the 6 months after diagnosis of heart failure in the past decade: population-based data from the UK.

Paresh A Mehta; Simon W Dubrey; Hugh F. McIntyre; David Walker; Suzanna M C Hardman; George C. Sutton; Theresa McDonagh; Martin R. Cowie

Objective: To investigate the secular trend in survival after a new diagnosis of heart failure in the UK population. Design and Setting: Comparison of all-cause mortality in the 6 months after diagnosis of heart failure in population-based studies in the south east of England in 2004–5 (Hillingdon–Hastings Study) and 1995–7 (Hillingdon–Bromley Studies). Participants: 396 patients in the 2004–5 cohort and 552 patients in the 1995–7 cohort with incident (new) heart failure. Main Outcome Measures: All-cause mortality. Results: All-cause mortality rates were 6% (95% CI 3% to 8%) at 1 month, 11% (8% to 14%) at 3 months and 14% (11% to 18%) at 6 months in the 2004–5 cohort compared with 16% (13% to 20%), 22% (19% to 25%) and 26% (22% to 29%), respectively, in the 1995–7 cohort (difference between the two cohorts, p<0.001). The difference in survival was not explained by any difference in the demographics or severity of heart failure at presentation. There was a difference at baseline and thereafter in the use of neurohormonal antagonists (β-blockers and angiotensin-converting enzyme inhibitors). Conclusions: Although early mortality remains high among patients with newly diagnosed heart failure in the UK general population, there is strong evidence of a marked improvement in survival from 1995–7 to 2004–5, perhaps partly explained by an increased usage of neurohormonal antagonists.


European Journal of Heart Failure | 2016

Initiating sacubitril/valsartan (LCZ696) in heart failure: results of TITRATION, a double-blind, randomized comparison of two uptitration regimens.

Michele Senni; John J.V. McMurray; Rolf Wachter; Hugh F. McIntyre; Antonio Reyes; Ivan Majercak; Peter Andreka; Nina Shehova-Yankova; Inder S. Anand; Mehmet Birhan Yilmaz; Harinder Gogia; Manuel Martínez-Sellés; Steffen Fischer; Zsolt Zilahi; Franco Cosmi; Valeri Gelev; Enrique Galve; Juanjo J. Gómez-Doblas; Jan Nociar; Maria Radomska; Beata Sokolova; Maurizio Volterrani; Arnab Sarkar; Bernard Reimund; Fabian Chen; Alan Charney

To assess the tolerability of initiating/uptitrating sacubitril/valsartan (LCZ696) from 50 to 200 mg twice daily (target dose) over 3 and 6 weeks in heart failure (HF) patients (ejection fraction ≤35%).


European Journal of Heart Failure | 2011

Leveraging guidelines: understanding heart failure, organizing care. Commentary on the 2010 NICE chronic heart failure guideline update.

Hugh F. McIntyre

Guidelines are written for clinicians. The uneven uptake of recommendations to date may reflect ambivalence in the clinician’s perception of the status of ‘guidance’, a vulnerability to new evidence and academic disparagement, and a lack of systematic guideline empowerment. As the current political and fiscal environment drives a reappraisal of healthcare organization, with a focus on commissioning ‘Quality’, the role of guidelines may be changing. The National Institute for Health and Clinical Effectiveness (NICE) recently published an updated version of the 2003 chronic heart failure guidelines. Following a pre-specified scope directing independent analysis of evidence, several new recommendations have been produced (Box 1). The purpose of these recommendations can broadly be summarized through two interlinked themes. The first and most immediate is the need for optimization; of the diagnostic opportunity, of the therapeutic strategy and of the organization of care. The second is a more conceptual need for greater understanding of the broader issue of the ‘congestive syndrome’, which increasingly predominates in ageing populations. The diagnosis of heart failure is often opportunistic, and frequently delayed. In diagnosing heart failure, no specific strategy had been recommended in the 2003 guidance, with use of natriuretic peptides (NP) seen as an optional adjunct to the electrocardiogram. Uptake was limited. On the basis of new data, a health technology analysis of NP, and evidence of persistent early attrition following the diagnosis of heart failure, direct referral for echocardiography and specialist assessment is now recommended for patients with suspected heart failure and a history of prior myocardial infarction (MI). This should occur within 2 weeks. Where MI has not occurred, NP should be measured, with the urgency of referral dictated by the degree of NP elevation. Concern has been expressed over the demand this may place upon services, however, the prognostic power of NP (a ‘death hormone’ to one independent expert), was felt by the guideline group to demand a response time at least comparable with the perhaps less ‘malignant’ cancers, for which 2 week referral is mandatory in England. While most therapies for left ventricular systolic dysfunction (LVSD) are well-established, randomized controlled trials published since 2003 have clarified the role and timing of medications; device therapy lies within another review area. The revised guidelines now recommend the combination of both angiotensinconverting enzyme (ACE) inhibitors (or angiotensin-receptor blockers if truly intolerant) and beta-blockers as ‘first line’ therapy. In common with other guidelines the addition of ‘second line’ treatment with an aldosterone antagonist, angiotensin-receptor blocker or the combination of nitrate and hydralazine should be considered, in appropriate populations, if symptoms persist. Although heart failure with preserved ejection fraction (HFpEF) is recognized as an increasing problem, it remains poorly understood. The absence of any treatment recommendations reflects the lack of benefit seen in limited studies to date. For all patients with heart failure, the importance of physical activity, with emotional and psychological support, is reflected in a new recommendation that patients should be included in group, exercise-based rehabilitation programmes. While supported by a strong evidence base, the variability of the exercise regimens reviewed precluded the identification of any specific methodology. The potential benefits of earlier diagnosis and optimal treatment are mediated through the context in which care is delivered. Evidence that both specialist supervision and nurse-led management programmes improve outcome is recognized in the updated recommendation that the initial diagnosis should be made by a specialist (in conjunction with formal echocardiographic assessment). Specialist supervision is also recommended where symptoms persist or worsen, or the patient is hospitalized. The updated definition of specialist (Box 2) is the product of lengthy interaction between external stakeholders and the eight clinicians on the group (one epidemiologist, one physician, one specialist heart failure nurse, two general practitioners, and three cardiologists). While healthcare systems may argue over whom best


Heart | 2002

Across the interface: the Hastings Heart Function Clinic

Hugh F. McIntyre; J Barrett; S Murphy; R Wray; S J Sutcliffe; David Walker

Heart failure is a descriptive clinical syndrome, which encompasses the consequences of both right and left ventricular dysfunction (systolic and non-systolic). Systolic left ventricular dysfunction, about which there is most epidemiological and experimental evidence, is a malignant disease. In a recent population based study more than one third of patients had died within 12 months of diagnosis.1 Estimates of the prevalence of systolic left ventricular dysfunction range from 3–20 per 1000 in the general population. Over the age of 65 this value rises to 30–130 per 1000.2 The true prevalence of the syndrome of heart failure is probably significantly higher, because of asymptomatic systolic left ventricular dysfunction and of “diastolic” (or non-systolic) left ventricular dysfunction. Taking a crude prevalence of systolic left ventricular dysfunction of 2% suggests that one million people are affected in the UK. Two thirds will die within five years. Despite this, to date heart failure has received less attention than its cancerous counterparts (table 1).3 This contrast is highlighted by the recent recommendation of a two week maximum on the time patients with suspected cancer should wait for review. View this table: Table 1 The incidence and prognosis of heart failure and common cancers in the Scotland3 The number of heart failure cases is likely to rise. This is because of the successful management of ischaemic heart disease, which serves to defer a cohort of cardiac morbidity, the better management of patients who already have heart failure, and the increasing numbers of elderly patients in the population. Elderly patients with heart failure are often taking several medications and have little understanding of their condition.4 They are frequently readmitted, often because of poor symptom control and reduced compliance.5 Several highly effective treatments exist for heart failure and authoritative guidelines have been produced.6,7 Despite the …


European Journal of Heart Failure | 2018

Impact of systolic blood pressure on the safety and tolerability of initiating and up-titrating sacubitril/valsartan in patients with heart failure and reduced ejection fraction: insights from the TITRATION study

Michele Senni; John J.V. McMurray; Rolf Wachter; Hugh F. McIntyre; Inder S. Anand; Vincenzo Duino; Arnab Sarkar; Victor Shi; Alan Charney

The TITRATION trial investigated two strategies to initiate and up‐titrate sacubitril/valsartan (LCZ696) to the same target dose, over a condensed (3‐week) or conservative (6‐week) period, in patients with heart failure with reduced ejection fraction (HFrEF) and systolic blood pressure (SBP) of ≥100 mmHg. This post hoc analysis examined the relationship between baseline SBP at screening and achievement of the target dose of sacubitril/valsartan of 97 mg/103 mg (also termed ‘LCZ696 200 mg’) twice per day during the study.


International Journal of Clinical Practice | 2009

Single‐pill combination therapy in hypertension: a rational or emotional construct?

Hugh F. McIntyre; P. M. Haydock

coronary artery bypass surgery. Scand Cardiovasc J 2003; 37: 309–15. 15 Magee MJ, Herbert MA, Dewey TM et al. Atrial fibrillation after coronary artery bypass grafting surgery: development of a predictive risk algorithm. Ann Thorac Surg 2007; 83: 1707–12; discussion 12. 16 Ahlsson A, Bodin L, Fengsrud E, Englund A. Patients with postoperative atrial fibrillation have a doubled cardiovascular mortality. Scand Cardiovasc J 2009; 12: 1–7. 17 Mathew JP, Fontes ML, Tudor IC et al. A multicenter risk index for atrial fibrillation after cardiac surgery. JAMA 2004; 291: 1720–9. 18 Stenestrand U, Lindback J, Wallentin L. Anticoagulation therapy in atrial fibrillation in combination with acute myocardial infarction influences long-term outcome: a prospective cohort study from the Register of Information and Knowledge About Swedish Heart Intensive Care Admissions (RIKS-HIA). Circulation 2005; 112: 3225–31. 19 Wong CK, White HD, Wilcox RG et al. Significance of atrial fibrillation during acute myocardial infarction, and its current management: insights from the GUSTO-3 trial. Card Electrophysiol Rev 2003; 7: 201–7. 20 Pedersen OD, Abildstrom SZ, Ottesen MM et al. Increased risk of sudden and non-sudden cardiovascular death in patients with atrial fibrillation ⁄ flutter following acute myocardial infarction. Eur Heart J 2006; 27: 290–5. 21 Hallberg P, Lindback J, Lindahl B et al. Digoxin and mortality in atrial fibrillation: a prospective cohort study. Eur J Clin Pharmacol 2007; 63: 959–71. 22 Fauchier L, Grimard C, Pierre B et al. Comparison of beta blocker and digoxin alone and in combination for management of patients with atrial fibrillation and heart failure. Am J Cardiol 2009; 103: 248–54.


International Journal of Clinical Practice | 2007

Lighting the vascular fuse – late surgical attrition in older patients

Hugh F. McIntyre

References 1 Lawson W, Hui J, Kennard E et al. Effect of enhanced external counterpulsation on medically refractory angina patients with erectile dysfunction. Int J Clin Pract 2007; 61: 757–62. 2 Werner D. Pneumatic external counterpulsation: a new non-invasive method to improve organ perfusion. Am J Card 1999; 84: 950–2. 3 Qian XX, Wu WK, Zheng ZS et al. Effect of enhanced external counterpulsation on nitric oxide production in coronary disease. J Heart Dis 1999; 1: 193 (A769). 4 Lawson WE, Hui JCK, Zheng ZS et al. Improved exercise tolerance following enhanced external counterpulsation: cardiac or peripheral effect? Cardiology 1996; 87: 1–5. 5 Bonetti PO, Barness GW, Keelan PC et al. Enhanced external counterpulsation improves endothelial function in patients with symptomatic coronary artery disease. JACC 2003; 41: 1761–8. 6 Bonetti PO, Gadasalli SN, Lerman A et al. Successful treatment of symptomatic coronary endothelial dysfunction with enhanced external counterpulsation. Mayo Clin Proc 2004; 79: 690–2. 7 Friccione GL, Jaghab K, Lawson W et al. Psychosocial effects of enhanced external counterpulsation in the angina patient. Psychosomatics 1995; 36: 494–7. 8 Greenstein A, Chen J, Miller H et al. Does severity of ischaemic coronary disease correlate with erectile dysfunction? Int J Impot Res 1997; 9: 123–6. 9 O’Kane PD, Jackson G. Erectile dysfunction: is there silent obstructive coronary artery disease? Int J Clin Pract 2001; 55: 219–20. 10 Kirby M, Jackson G, Betteridge J et al. Is erectile dysfunction a marker for cardiovascular disease? Int J Clin Pract 2001; 155: 614–8. 11 Jackson G, Rosen RC, Kloner RA et al. The second Princeton consensus on sexual dysfunction and cardiac risk: new guidelines for sexual medicine. J Sex Med 2006; 3: 28–36. 12 Padma-Nathan H, Eardley I, Kloner R et al. A 4-year update on the safety of sildenafil citrate (Viagra). Urology 2002; 60 (Suppl. 2B): 67–90. 13 Emmick JT, Stuewe SR, Mitchell M. Overview of the cardiovascular effects of tadalafil. Eur Heart J 2002; 4 (Suppl. H): H32– 47. 14 Webb DJ, Freestone S, Allen MJ et al. Sildenafil citrate and bloodpressure-lowering drugs: results of drug interaction studies with an organic nitrate and a calcium antagonist. Am J Cardiol 1999; 83: 21C–8C. 15 Arruda-Olsen AM, Mahoney DW, Nehra A et al. Cardiovascular effects of sildenafil during exercise in men with known or probable coronary artery disease: a randomised crossover trial. JAMA 2002; 287: 719–25. 16 Hermann HC, Chang G, Klugherz BD et al. Haemodynamic effects of sildenafil in men with severe coronary artery disease. N Engl J Med 2000; 342: 1622–6. 17 Jackson G, Benjamin N, Jackson N et al. Effects of sildenafil citrate on human haemodynamics. Am J Cardiol 1999; 83: 13C– 20C. 18 Arruda-Olsen AM, Mahoney DW, Nehra A et al. Cardiovascular effects of sildenafil during exercise in men with known or probable coronary artery disease. JAMA 2002; 287: 719–25. 19 Jaarsma T, Dracup K, Walden J et al. Sexual function in patients with advanced heart failure. Heart Lung 1996; 25: 262–70. 20 Hare JM, Colucci WS. Role of nitric oxide in the regulation of myocardial function. Prog Cardiovasc Dis 1995; 38: 155–66. 21 Katz SD, Balidemaj K, Homma S et al. Acute type-5 phosphodiesterase inhibition with sildenafil enhances flow-mediated vasodilation in patients with chronic heart failure. J Am Coll Cardiol 2000; 36: 845–51. 22 Negrao CE, Hamilton MA, Fonarow GC et al. Impaired endothelium-mediated vasodilation is not eh principla cause of vasoconstriction in heart failure. Am J Physiol Heart Circ Physiol 2000; 278: H168–H74. 23 de Wit C, Bolz SS, Pohl U. Interaction of endothelial autocoids in microvascular control. Z Kardiol 2000; 99: 255–60. 24 Vallance P, Collier J, Moncada S. Effects of endothelium-derived nitric oxide on peripheral arteriolar tone in man. Lancet 1989; 2: 997–1000. 25 Haynes WG, Noon JP, Walker BR et al. Inhibition of nitric oxide synthesis increases blood pressure in healthy humans. J Hypertens 1993; 11: 1375–80. 26 Bech JN, Nielsen CB, Penderson EB. Effects of systemic NO synthesis inhibition on RPF, GFR, UNa and vasoactive hormones in healthy humans. Am J Physiol 1996; 270: F845–51.

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George C. Sutton

National Institutes of Health

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Ali Vazir

National Institutes of Health

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Mary J. Morrell

National Institutes of Health

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