Publications by authors named "Edward D Frohlich"

Objective: To determine the association of post-traumatic stress disorder (PTSD) symptoms following Hurricane Katrina with incident cardiovascular disease (CVD) events in older, hypertensive, community-dwelling adults both overall and stratified by age, sex, and race.

Methods: This was a prospective cohort study performed in Southeastern Louisiana 12-24 months following Hurricane Katrina through February 2011. Participants were community-dwelling older adults (n = 2,073) enrolled in the Cohort Study of Medication Adherence Among Older Adults with no known history of CVD events.

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The changes in American academic medicine in the last 6 decades has been a success. During these years, I participated in this development through patients care, research, editorship of major Journals and as a member of governing boards of several professional organizations. This discussion will describe some of the developments of medicine and will recount my own professional career and my mentors who help me to achieve my goals.

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This article provides a preview to the forthcoming articles in this issue, which are written by well-known and authoritative authors for the readers' pleasure and reference. This article hopes to provide a general overview that stimulates interest, better understanding, and continued joint commitment to the important subject of hypertension.

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Background: Many epidemiological, clinical, and experimental reports have demonstrated an association between serum uric acid concentration and a variety of cardiovascular and renal diseases, particularly in hypertension. At present, there seems to be no resolution to the question whether this relationship is causal or coincidental.

Summary: This discussion examines a number of biological, pathophysiological, fundamental, and clinical relationships between serum uric acid concentration and several of these disorders.

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Background: Pharmacy refill adherence assesses the medication-filling behaviors, whereas self-report adherence assesses the medication-taking behaviors. We contrasted the association of pharmacy refill and self-reported antihypertensive medication adherence with blood pressure (BP) control and cardiovascular disease (CVD) incidence.

Methods And Results: Adults (n = 2075) from the prospective Cohort Study of Medication Adherence among Older Adults recruited between August 2006 and September 2007 were included.

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Excessive dietary salt intake induces extensive cardiovascular and renal damage in spontaneously hypertensive rats (SHR) that may be prevented by antihypertensive agents. This study examines whether salt-induced cardiac damage may be reversed by angiotensin II (type 1) receptor blockade (telmisartan). Eight-week-old male SHRs were divided into four groups; Group 1 (NS) was fed regular rat chow, and Group 2 (HS) received high-salt diet (HS; 8% NaCl).

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Evidence for the potential role of organ specific cardiovascular renin-angiotensin systems (RAS) has been demonstrated experimentally and clinically with respect to certain cardiovascular and renal diseases. These findings have been supported by studies involving pharmacological inhibition during ischemic heart disease, myocardial infarction, cardiac failure; hypertension associated with left ventricular ischemia, myocardial fibrosis and left ventricular hypertrophy; structural and functional changes of the target organs associated with prolonged dietary salt excess; and intrarenal vascular disease associated with end-stage renal disease. Moreover, the severe structural and functional changes induced by these pathological conditions can be prevented and reversed by agents producing RAS inhibition (even when not necessarily coincident with alterations in arterial pressure).

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Recent reports of selected observational studies and a meta-analysis have stirred controversy and have become the impetus for calls to abandon recommendations for reduced sodium intake by the US general population. A detailed review of these studies documents substantial methodological concerns that limit the usefulness of these studies in setting, much less reversing, dietary recommendations. Indeed, the evidence base supporting recommendations for reduced sodium intake in the general population remains robust and persuasive.

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Background: We have demonstrated previously that a high-salt diet (HS) produces myocardial fibrosis, left ventricular (LV) dysfunction, and renal insufficiency in adult spontaneously hypertensive rats (SHR), and that blockade of the renin-angiotensin system prevented those adverse effects of HS.

Methods And Results: Eight-week-old male SHR were divided into four groups: controls received regular rat chow (0.6 NaCl); the other three were given HS.

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The effects of angiotensin receptor blocker, diuretic, a calcium antagonist, and their combination were evaluated on the progression of cardiovascular and renal damage in spontaneously hypertensive rats (SHRs) given excess salt. To this end, 8-week male SHRs were divided into 7 groups. The control group (C) received normal NaCl (0.

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This brief review discusses some aspects of hypertensive damage to the kidneys and cardiovascular system. A comparison of renal and cardiac manifestations of hypertensive disease between results of clinical and experimental studies was made, with a major focus on the possible role of salt and the renin-angiotensin system (RAS) in inducing target organ damage. Thus, some degree of renal impairment is often present in patients with essential hypertension, varying from microalbuminuria to end-stage renal disease, whereas in rats with spontaneous hypertension only slight renal damage is seen in old rats with little evidence of renal failure.

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Purpose Of Review: This review will discuss some relevant and novel studies on the relationship between sodium intake and cardiovascular structure and function, focusing on blood pressure independent effects of salt on the heart, arteries, and kidneys.

Recent Findings: Several new reports clearly demonstrate the role of high dietary salt in mediating cardiovascular and renal morbidity and mortality including stroke, myocardial infarction, arterial stiffening, heart failure, and renal insufficiency. A number of recent studies also indicate that in addition to increased sodium intake, simultaneous decrease in potassium intake may aggravate adverse cardiovascular and renal manifestations.

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Pressure overload.

Heart Fail Clin

January 2012

Article Synopsis
  • The review explores how pressure overload on the heart leads to ventricular hypertrophy as a compensatory mechanism to manage increased stress on the walls of the heart.
  • Although ventricular hypertrophy initially helps, it involves changes that can negatively affect heart function over time, potentially resulting in heart failure.
  • The text highlights specific molecular mechanisms that drive hypertrophy and can lead to harmful structural changes in the heart, increasing the risk of serious cardiac issues.
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Few data are available on the predictors of decline in antihypertensive medication adherence and the association of decline in adherence with subsequent blood pressure (BP) control. The current analysis included 1965 adults from the Cohort Study of Medication Adherence Among Older Adults recruited between August 2006 and September 2007. Decline in antihypertensive medication adherence was defined as a ≥2-point decrease on the 8-item Morisky Medication Adherence Scale assessed during telephone surveys 1 and 2 years after baseline.

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