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Dive into the research topics where Wazir Baig is active.

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Featured researches published by Wazir Baig.


Circulation | 1998

Prospective Study of Heart Rate Variability and Mortality in Chronic Heart Failure Results of the United Kingdom Heart Failure Evaluation and Assessment of Risk Trial (UK-Heart)

James Nolan; Phillip D. Batin; Richard Andrews; Steven J. Lindsay; Paul Brooksby; Michael Mullen; Wazir Baig; Andrew D. Flapan; A.J. Cowley; Robin Prescott; James M.M. Neilson; Keith A.A. Fox

BACKGROUND Patients with chronic heart failure (CHF) have a continuing high mortality. Autonomic dysfunction may play an important role in the pathophysiology of cardiac death in CHF. UK-HEART examined the value of heart rate variability (HRV) measures as independent predictors of death in CHF. METHODS AND RESULTS In a prospective study powered for mortality, we recruited 433 outpatients 62+/-9.6 years old with CHF (NYHA functional class I to III; mean ejection fraction, 0.41+/-0.17). Time-domain HRV indices and conventional prognostic indicators were related to death by multivariate analysis. During 482+/-161 days of follow-up, cardiothoracic ratio, SDNN, left ventricular end-systolic diameter, and serum sodium were significant predictors of all-cause mortality. The risk ratio for a 41.2-ms decrease in SDNN was 1.62 (95% CI, 1.16 to 2.44). The annual mortality rate for the study population in SDNN subgroups was 5.5% for >100 ms, 12.7% for 50 to 100 ms, and 51.4% for <50 ms. SDNN, creatinine, and serum sodium were related to progressive heart failure death. Cardiothoracic ratio, left ventricular end-diastolic diameter, the presence of nonsustained ventricular tachycardia, and serum potassium were related to sudden cardiac death. A reduction in SDNN was the most powerful predictor of the risk of death due to progressive heart failure. CONCLUSIONS CHF is associated with autonomic dysfunction, which can be quantified by measuring HRV. A reduction in SDNN identifies patients at high risk of death and is a better predictor of death due to progressive heart failure than other conventional clinical measurements. High-risk subgroups identified by this measurement are candidates for additional therapy after prescription of an ACE inhibitor.


Journal of the American College of Cardiology | 2002

Predicting death due to progressive heart failure in patients with mild-to-moderate chronic heart failure

Mark T. Kearney; Keith A.A. Fox; Amanda Lee; Robin Prescott; Ajay M. Shah; Philip D. Batin; Wazir Baig; Stephen Lindsay; Timothy S. Callahan; William E. Shell; Azfar Zaman; Simon G Williams; James M.M. Neilson; James Nolan

OBJECTIVES The aim of this study was to explore the value of noninvasive predictors of death/mode of death in ambulant outpatients with chronic heart failure (HF). BACKGROUND Mortality in chronic HF remains high, with a significant number of patients dying of progressive disease. Identification of these patients is important. METHODS We recruited 553 ambulant outpatients age 63 +/- 10 years with symptoms of chronic HF (New York Heart Association functional class, 2.3 +/- 0.5) and objective evidence of left ventricular dysfunction (ejection fraction <45%, cardiothoracic ratio >0.55, or pulmonary edema on chest radiograph). After 2,365 patient-years of follow-up, 201 patients had died, with 76 events due to progressive HF. RESULTS Independent predictors of all-cause mortality assessed with the Cox proportional hazards model were as follows: a low standard deviation of all normal-to-normal RR intervals (SDNN); lower serum sodium and higher creatinine levels; higher cardiothoracic ratio; nonsustained ventricular tachycardia; higher left ventricular end-systolic diameter; left ventricular hypertrophy; and increasing age. Independent predictors of death specific to progressive HF were SDNN, serum sodium and creatinine levels. The hazard ratio of progressive HF death for a 10% decrease in SDNN was 1.06 (95% confidence interval [CI], 1.01 to 1.12); for a 2 mmol/l decrease in serum sodium, 1.22 (95% CI, 1.08 to 1.38); and for a 10 micromol/l increase in serum creatinine, 1.14 (95% CI, 1.09 to 1.19) (all p < 0.01). CONCLUSIONS In ambulant outpatients with chronic HF, low serum sodium and SDNN and high serum creatinine identify patients at increased risk of death due to progressive HF.


Circulation-heart Failure | 2011

Changing Characteristics and Mode of Death Associated With Chronic Heart Failure Caused by Left Ventricular Systolic Dysfunction A Study Across Therapeutic Eras

Richard M. Cubbon; Chris Gale; Lorraine Kearney; Clyde B. Schechter; W. Paul Brooksby; James Nolan; Keith A.A. Fox; Adil Rajwani; Wazir Baig; David Groves; Pauline Barlow; Anthony C. Fisher; Phillip D. Batin; Matthew Kahn; Azfar Zaman; Ajay M. Shah; Jon A. Byrne; Steven J. Lindsay; Robert J. Sapsford; Stephen B. Wheatcroft; Klaus K. Witte; Mark T. Kearney

Background—Therapies for patients with chronic heart failure caused by left ventricular systolic dysfunction have advanced substantially over recent decades. The cumulative effect of these therapies on mortality, mode of death, symptoms, and clinical characteristics has yet to be defined. Methods and Results—This study was a comparison of 2 prospective cohort studies of outpatients with chronic heart failure caused by left ventricular systolic dysfunction performed between 1993 and 1995 (historic cohort: n=281) and 2006 and 2009 (contemporary cohort: n=357). In the historic cohort, 83% were prescribed angiotensin-converting enzyme inhibitors and 8.5% were prescribed &bgr;-adrenoceptor antagonists, compared with 89% and 80%, respectively, in the contemporary cohort. Mortality rates over the first year of follow-up declined from 12.5% to 7.8% between eras (P=0.04), and sudden death contributed less to contemporary mortality (33.6% versus 12.7%; P<0.001). New York Heart Association class declined between eras (P<0.001). QTc dispersion across the chest leads declined from 85 ms (SD, 2) to 34 ms (SD, 1) and left ventricular end-diastolic dimensions declined from 65 mm (SD, 0.6) to 59 mm (SD, 0.5) (both P<0.001). Conclusions—Survival has significantly improved in patients with chronic heart failure caused by left ventricular systolic dysfunction over the past 15 years; furthermore, sudden death makes a much smaller contribution to mortality, and noncardiac mortality is a correspondingly greater contribution. This has been accompanied by an improvement in symptoms and some markers of adverse electric and structural left ventricular remodeling.


Clinical Radiology | 2010

The MRI appearances of early vertebral osteomyelitis and discitis.

J.A.T. Dunbar; Jonathan Sandoe; A.S. Rao; D.W. Crimmins; Wazir Baig; J.J. Rankine

AIM To describe the magnetic resonance imaging (MRI) appearances in patients with a clinical history suggestive of vertebral osteomyelitis and discitis who underwent MRI very early in their clinical course. MATERIALS AND METHODS A retrospective review of the database of spinal infections from a spinal microbiological liaison team was performed over a 2 year period to identify cases with clinical features suggestive of spinal infection and an MRI that did not show features typical of vertebral osteomyelitis and discitis. All patients had positive microbiology and a follow up MRI showing typical features of spinal infection. RESULTS In four cases the features typical of spinal infection were not evident at the initial MRI. In three cases there was very subtle endplate oedema associated with disc degeneration, which was interpreted as Modic type I degenerative endplate change. Intravenous antibiotic therapy was continued prior to repeat MRI examinations. The mean time to the repeat examination was 17 days with a range of 8-22 days. The second examinations clearly demonstrated vertebral osteomyelitis and discitis. CONCLUSION Although MRI is the imaging method of choice for vertebral osteomyelitis and discitis in the early stages, it may show subtle, non-specific endplate subchondral changes; a repeat examination may be required to show the typical features.


Circulation-heart Failure | 2011

Changing Characteristics and Mode of Death Associated With Chronic Heart Failure Caused by Left Ventricular Systolic DysfunctionClinical Perspective

Richard M. Cubbon; Chris Gale; Lorraine Kearney; Clyde B. Schechter; W. Paul Brooksby; James Nolan; Keith A.A. Fox; Adil Rajwani; Wazir Baig; David Groves; Pauline Barlow; Anthony C. Fisher; Phillip D. Batin; Matthew Kahn; Azfar Zaman; Ajay M. Shah; Jon A. Byrne; Steven J. Lindsay; Robert J. Sapsford; Stephen B. Wheatcroft; Klaus K. Witte; Mark T. Kearney

Background—Therapies for patients with chronic heart failure caused by left ventricular systolic dysfunction have advanced substantially over recent decades. The cumulative effect of these therapies on mortality, mode of death, symptoms, and clinical characteristics has yet to be defined. Methods and Results—This study was a comparison of 2 prospective cohort studies of outpatients with chronic heart failure caused by left ventricular systolic dysfunction performed between 1993 and 1995 (historic cohort: n=281) and 2006 and 2009 (contemporary cohort: n=357). In the historic cohort, 83% were prescribed angiotensin-converting enzyme inhibitors and 8.5% were prescribed &bgr;-adrenoceptor antagonists, compared with 89% and 80%, respectively, in the contemporary cohort. Mortality rates over the first year of follow-up declined from 12.5% to 7.8% between eras (P=0.04), and sudden death contributed less to contemporary mortality (33.6% versus 12.7%; P<0.001). New York Heart Association class declined between eras (P<0.001). QTc dispersion across the chest leads declined from 85 ms (SD, 2) to 34 ms (SD, 1) and left ventricular end-diastolic dimensions declined from 65 mm (SD, 0.6) to 59 mm (SD, 0.5) (both P<0.001). Conclusions—Survival has significantly improved in patients with chronic heart failure caused by left ventricular systolic dysfunction over the past 15 years; furthermore, sudden death makes a much smaller contribution to mortality, and noncardiac mortality is a correspondingly greater contribution. This has been accompanied by an improvement in symptoms and some markers of adverse electric and structural left ventricular remodeling.


BJUI | 2014

A case-control study: are urological procedures risk factors for the development of infective endocarditis?

Amar Mohee; Robert West; Wazir Baig; Ian Eardley; Jonathan Sandoe

To evaluate the association between urological procedures and the development of infective endocarditis (IE), as there are case‐reports linking urological procedures to IE but evidence of a causal relationship is lacking and no major guidelines advise prophylaxis to prevent development of IE during transurethral urological procedures. No case‐control study has been undertaken to examine the relationship between urological procedures and the development of IE.


Journal of Hospital Infection | 2013

Vascular access strategy for delivering long-term antimicrobials to patients with infective endocarditis: device type, risk of infection and mortality

F.Z. Ahmed; Wazir Baig; Theresa Munyombwe; Robert West; Jonathan Sandoe

BACKGROUND This paper reports the use of different vascular access devices and the incidence of intravascular catheter-related infection (CRI) in patients receiving intravenous antibiotics for infective endocarditis (IE). AIM To examine whether rates of infection vary with type of vascular access device, and assess the impact of CRI on mortality in IE. METHODS A prospective observational service evaluation of all inpatients who received intravenous antibiotics for IE was performed. In total, 114 inpatients were evaluated. All cases of CRI [including exit-site infection, intravascular catheter-related bloodstream infection (CRBSI) and mortality] were recorded. Tunnelled and non-tunnelled central venous catheters (CVCs), and peripherally inserted cannulae were used for antibiotic delivery. FINDINGS There were 15 episodes of CRI, 11 of which were CRBSI (all associated with CVC use). The remainder comprised uncomplicated exit-site infections. Use of tunnelled CVCs [hazard ratio (HR) 16.95, 95% confidence interval (CI) 2.13-134.93; P = 0.007] and non-tunnelled CVCs (HR 24.54, 95% CI 2.83-212.55; P = 0.004) was associated with a significantly increased risk of CRI. Risk of mortality increased significantly with Staphylococcus aureus as the cause of IE (P < 0.001) and CRBSI (P = 0.034). CONCLUSION Risk of CRI in patients with IE is linked to the type of vascular access device used. Rates of CRBSI were greatest with CVCs, while peripheral venous cannulae were not associated with CRBSI or serious sequelae. Many patients (40%) tolerated complete treatment courses delivered via peripheral cannulae. These findings confirm the importance of device selection in reducing the risk of CRI; a potentially modifiable variable that impacts on outcome and mortality in IE.


Future Cardiology | 2012

Indications for daptomycin use in endocarditis and pacemaker lead infection and outcomes in Leeds, UK

Jonathan Sandoe; Wazir Baig

Infective endocarditis now comprises an increasingly complex mixture of endocardial infections, with staphylococci as the predominant cause. Although vancomycin has been an important therapeutic option for several decades, reduced susceptibility is emerging. Daptomycin is a relatively new antimicrobial agent, approved for right-sided endocarditis, but the data for other forms of endocarditis are limited. Here we report clinical data from the Leeds Endocarditis Service (Leeds, UK) for 19 patients treated with daptomycin between January 2007 and December 2009. The majority of cases were caused by staphylococci. All patients were treated with 6 mg/kg with a median treatment duration of 29 days. In total, 53% of patients were cured with antimicrobial regimens, which included daptomycin. Four patients (21%) died during therapy or within 30 days of stopping treatment. The current series is representative of everyday clinical practice and reflects the current difficulties in managing endocarditis.


Circulation-heart Failure | 2011

Changing Characteristics and Mode of Death Associated with Chronic Heart Failure Due to Left Ventricular Systolic Dysfunction: A Study Across Therapeutic Eras

Richard M. Cubbon; Chris Gale; Lorraine Kearney; Clyde B. Schechter; W. Paul Brooksby; James Nolan; Keith A.A. Fox; Adil Rajwani; Wazir Baig; David Groves; Pauline Barlow; Anthony C. Fisher; Phillip D. Batin; Matthew Kahn; Azfar Zaman; Ajay M. Shah; Jon A. Byrne; Steven J. Lindsay; Robert J. Sapsford; Stephen B. Wheatcroft; Klaus K. Witte; Mark T. Kearney

Background—Therapies for patients with chronic heart failure caused by left ventricular systolic dysfunction have advanced substantially over recent decades. The cumulative effect of these therapies on mortality, mode of death, symptoms, and clinical characteristics has yet to be defined. Methods and Results—This study was a comparison of 2 prospective cohort studies of outpatients with chronic heart failure caused by left ventricular systolic dysfunction performed between 1993 and 1995 (historic cohort: n=281) and 2006 and 2009 (contemporary cohort: n=357). In the historic cohort, 83% were prescribed angiotensin-converting enzyme inhibitors and 8.5% were prescribed &bgr;-adrenoceptor antagonists, compared with 89% and 80%, respectively, in the contemporary cohort. Mortality rates over the first year of follow-up declined from 12.5% to 7.8% between eras (P=0.04), and sudden death contributed less to contemporary mortality (33.6% versus 12.7%; P<0.001). New York Heart Association class declined between eras (P<0.001). QTc dispersion across the chest leads declined from 85 ms (SD, 2) to 34 ms (SD, 1) and left ventricular end-diastolic dimensions declined from 65 mm (SD, 0.6) to 59 mm (SD, 0.5) (both P<0.001). Conclusions—Survival has significantly improved in patients with chronic heart failure caused by left ventricular systolic dysfunction over the past 15 years; furthermore, sudden death makes a much smaller contribution to mortality, and noncardiac mortality is a correspondingly greater contribution. This has been accompanied by an improvement in symptoms and some markers of adverse electric and structural left ventricular remodeling.


Circulation-heart Failure | 2011

Changing Characteristics and Mode of Death Associated With Chronic Heart Failure Caused by Left Ventricular Systolic Dysfunction

Richard M. Cubbon; Chris Gale; Lorraine Kearney; Clyde B. Schechter; W. Paul Brooksby; James Nolan; Keith A.A. Fox; Adil Rajwani; Wazir Baig; David Groves; Pauline Barlow; Anthony C. Fisher; Phillip D. Batin; Matthew Kahn; Azfar Zaman; Ajay M. Shah; Jon A. Byrne; Steven J. Lindsay; Robert J. Sapsford; Stephen B. Wheatcroft; Klaus K. Witte; Mark T. Kearney

Background—Therapies for patients with chronic heart failure caused by left ventricular systolic dysfunction have advanced substantially over recent decades. The cumulative effect of these therapies on mortality, mode of death, symptoms, and clinical characteristics has yet to be defined. Methods and Results—This study was a comparison of 2 prospective cohort studies of outpatients with chronic heart failure caused by left ventricular systolic dysfunction performed between 1993 and 1995 (historic cohort: n=281) and 2006 and 2009 (contemporary cohort: n=357). In the historic cohort, 83% were prescribed angiotensin-converting enzyme inhibitors and 8.5% were prescribed &bgr;-adrenoceptor antagonists, compared with 89% and 80%, respectively, in the contemporary cohort. Mortality rates over the first year of follow-up declined from 12.5% to 7.8% between eras (P=0.04), and sudden death contributed less to contemporary mortality (33.6% versus 12.7%; P<0.001). New York Heart Association class declined between eras (P<0.001). QTc dispersion across the chest leads declined from 85 ms (SD, 2) to 34 ms (SD, 1) and left ventricular end-diastolic dimensions declined from 65 mm (SD, 0.6) to 59 mm (SD, 0.5) (both P<0.001). Conclusions—Survival has significantly improved in patients with chronic heart failure caused by left ventricular systolic dysfunction over the past 15 years; furthermore, sudden death makes a much smaller contribution to mortality, and noncardiac mortality is a correspondingly greater contribution. This has been accompanied by an improvement in symptoms and some markers of adverse electric and structural left ventricular remodeling.

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Jonathan Sandoe

Leeds Teaching Hospitals NHS Trust

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Chris Gale

Imperial College London

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