Keith C. Ferdinand

Dr. Keith C. Ferdinand


Research Focus & Metrics

Academic Career Length

15Years (2012-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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30 August 2017 in The Journal of Clinical Hypertension
Verified
Journal Article
Open access
PDF file
KFKeith C. Ferdinand
Keith C. Ferdinand
KYKapil Yadav
Kapil Yadav
SNSamar A. Nasser
Samar A. Nasser
HCHelene D. Clayton‐Jeter
Helene D. Clayton‐Jeter
JLJohn Lewin
John Lewin
FSFortunato Fred Senatore
Fortunato Fred Senatore
Blacks are two to three times as likely as whites to die of preventable heart disease and stroke. Declines in mortality from heart disease have not eliminated racial disparities. Control and effective treatment of hypertension, a leading cause of cardiovascular disease, among blacks is less than in whites and remains a challenge. One of the driving forces behind this racial/ethnic disparity is medication nonadherence whose cause is embedded in social determinants. Eight practical approaches to addressing medication adherence with the potential to attenuate disparities were identified and include: (1) patient engagement strategies, (2) consumer‐directed health care, (3) patient portals, (4) smart apps and text messages, (5) digital pillboxes, (6) pharmacist‐led engagement, (7) cardiac rehabilitation, and (8) cognitive‐based behavior. However, while data suggest that these strategies may improve medication adherence, the effect on ameliorating racial/ethnic disparities is not certain. This review describes the relationship between disparities and medication adherence, which likely plays a role in persistent disparities in cardiovascular morbidity and mortality.

1 December 2021 in JACC
Verified
Journal Article
Closed access
MOModele O. Ogunniyi
Modele O. Ogunniyi
YCYvonne Commodore-Mensah
Yvonne Commodore-Mensah
KFKeith C. Ferdinand
Keith C. Ferdinand

1 October 2014 in Hypertension
Verified
Journal Article
Closed access
KFKeith C. Ferdinand
Keith C. Ferdinand
WWWilliam B. White
William B. White
DCDavid A. Calhoun
David A. Calhoun
ELEva M. Lonn
Eva M. Lonn
PSPhilip T. Sager
Philip T. Sager
MGMary Jane Geiger
Mary Jane Geiger
Glucagon-like peptide-1 receptor agonists, used to treat type 2 diabetes mellitus, are associated with small reductions in systolic blood pressure (SBP) and increases in heart rate. However, findings based on clinic measurements do not adequately assess a drug’s 24-hour pharmacodynamic profile. The effects of dulaglutide, a once-weekly glucagon-like peptide-1 receptor agonist, on BP and heart rate were investigated using ambulatory BP monitoring. Patients (n=755; 56±10 years; 81% white; 48% women), with type 2 diabetes mellitus, taking ≥1 oral antihyperglycemic medication, with a clinic BP between 90/60 and 140/90 mm Hg were randomized to dulaglutide (1.5 or 0.75 mg) or placebo subcutaneously for 26 weeks. Ambulatory BP monitoring was performed at baseline and at 4, 16, and 26 weeks. The primary end point was change from baseline to week 16 in mean 24-hour SBP, a tree gatekeeping strategy compared the effects of dulaglutide to placebo. Both doses of dulaglutide were noninferior to placebo for changes in 24-hour SBP and diastolic blood pressure, and dulaglutide 1.5 mg significantly reduced SBP (least squares mean difference [95% confidence interval]), −2.8 mm Hg [−4.6, −1.0]; P ≤0.001). Dulaglutide 0.75 mg was noninferior to placebo (1.6 bpm; [0.3, 2.9]; P ≤0.02) for 24-hour heart rate (least squares mean difference [95% confidence interval]), but dulaglutide 1.5 mg was not (2.8 bpm [1.5, 4.2]). Dulaglutide 1.5 mg was associated with a reduction in 24-hour SBP and an increase in 24-hour heart rate. The mechanisms responsible for the observed effects remain to be clarified.

1 October 2024 in Hypertension
Verified
Journal Article
Open access
JCJennifer L. Cluett
Jennifer L. Cluett
OBOlivia Blazek
Olivia Blazek
ABAngela L. Brown
Angela L. Brown
CECara East
Cara East
KFKeith C. Ferdinand
Keith C. Ferdinand
ODon behalf of the American Heart Association Council on Hypertension; Council on Cardiovascular and Stroke Nursing; Council on the Kidney in Cardiovascular Disease; and Council on Peripheral Vascular Disease
on behalf of the American Heart Association Council on Hypertension; Council on Cardiovascular and Stroke Nursing; Council on the Kidney in Cardiovascular Disease; and Council on Peripheral Vascular Disease
Hypertension is a leading risk factor for cardiovascular morbidity and mortality. Despite the widespread availability of both pharmacological and lifestyle therapeutic options, blood pressure control rates across the globe are worsening. In fact, only 23% of individuals with high blood pressure in the United States achieve treatment goals. In 2023, the US Food and Drug Administration approved renal denervation, a catheter-based procedure that ablates the renal sympathetic nerves, as an adjunctive treatment for patients in whom lifestyle modifications and antihypertensive medications do not adequately control blood pressure. This approval followed the publication of multiple randomized clinical studies using rigorous trial designs, all incorporating renal angiogram as the sham control. Most but not all of the new generation of trials reached their primary end point, demonstrating modest efficacy of renal denervation in lowering blood pressure across a spectrum of hypertension, from mild to truly resistant. Individual patient responses vary, and further research is needed to identify those who may benefit most. The initial safety profile appears favorable, and multiple ongoing studies are assessing longer-term efficacy and safety. Multidisciplinary teams that include hypertension specialists and adequately trained proceduralists are crucial to ensure that referrals are made appropriately with full consideration of the potential risks and benefits. Incorporating patient preferences and engaging in shared decision-making conversations will help patients make the best decisions given their individual circumstances. Although further research is clearly needed, renal denervation presents a novel treatment strategy for patients with uncontrolled blood pressure.

1 September 2023 in Annals of Internal Medicine
Verified
Journal Article
Closed access
JHJiang He
Jiang He
JBJoshua D. Bundy
Joshua D. Bundy
SGSiyi Geng
Siyi Geng
LTLing Tian
Ling Tian
HHHua He
Hua He
JCJing Chen
Jing Chen
Cardiovascular disease (CVD) mortality is persistently higher in the Black population than in other racial and ethnic groups in the United States. To examine the degree to which social, behavioral, and metabolic risk factors are associated with CVD mortality and the extent to which racial differences in CVD mortality persist after these factors are accounted for. Prospective cohort study. NHANES (National Health and Nutrition Examination Survey) 1999 to 2018. A nationally representative sample of 50 808 persons aged 20 years or older. Data on social, behavioral, and metabolic factors were collected in each NHANES survey using standard methods. Deaths from CVD were ascertained from linkage to the National Death Index with follow-up through 2019. Over an average of 9.4 years of follow-up, 2589 CVD deaths were confirmed. The age- and sex-standardized rates of CVD mortality were 484.7 deaths per 100 000 person-years in Black participants, 384.5 deaths per 100 000 person-years in White participants, 292.4 deaths per 100 000 person-years in Hispanic participants, and 255.1 deaths per 100 000 person-years in other race groups. In a multiple Cox regression analysis adjusted for all measured risk factors simultaneously, several social (unemployment, low family income, food insecurity, lack of home ownership, and unpartnered status), behavioral (current smoking, lack of leisure-time physical activity, and sleep 8 h/d), and metabolic (obesity, hypertension, and diabetes) risk factors were associated with a significantly higher risk for CVD death. After adjustment for these metabolic, behavioral, and social risk factors separately, hazard ratios of CVD mortality for Black compared with White participants were attenuated from 1.54 (95% CI, 1.34 to 1.77) to 1.34 (CI, 1.16 to 1.55), 1.31 (CI, 1.15 to 1.50), and 1.04 (CI, 0.90 to 1.21), respectively. Causal contributions of social, behavioral, and metabolic risk factors to racial and ethnic disparities in CVD mortality could not be established. The Black-White difference in CVD mortality diminished after adjustment for behavioral and metabolic risk factors and completely dissipated with adjustment for social determinants of health in the U.S. population. National Institutes of Health.

12 June 2020 in Journal of Medical Virology
Verified
Journal Article
Open access
PDF file
ETEman Toraih
Eman Toraih
Rami ElshazliRami Elshazli
Rami Elshazli
MHMohamed Hussein
Mohamed Hussein
Abdelaziz ElgamlAbdelaziz Elgaml
Abdelaziz Elgaml
MAMohamed Amin
Mohamed Amin
Manal S. FawzyManal S. Fawzy
Manal S. Fawzy
Background: Coronavirus disease‐2019 (COVID‐19) has a deleterious effect on several systems, including the cardiovascular system. We aim to systematically explore the association of COVID‐19 severity and mortality rate with the history of cardiovascular diseases and/or other comorbidities and cardiac injury laboratory markers.Methods: The standardized mean difference (SMD) or odds ratio (OR) and 95% confidence intervals (CIs) were applied to estimate pooled results from the 56 studies. The prognostic performance of cardiac markers for predicting adverse outcomes and to select the best cutoff threshold was estimated by receiver operating characteristic curve analysis. Decision tree analysis by combining cardiac markers with demographic and clinical features was applied to predict mortality and severity in patients with COVID‐19.Results: A meta‐analysis of 17 794 patients showed patients with high cardiac troponin I (OR = 5.22, 95% CI = 3.73‐7.31, P < .001) and aspartate aminotransferase (AST) levels (OR = 3.64, 95% CI = 2.84‐4.66, P < .001) were more likely to develop adverse outcomes. High troponin I more than 13.75 ng/L combined with either advanced age more than 60 years or elevated AST level more than 27.72 U/L was the best model to predict poor outcomes.Conclusions: COVID‐19 severity and mortality are complicated by myocardial injury. Assessment of cardiac injury biomarkers may improve the identification of those patients at the highest risk and potentially lead to improved therapeutic approaches.