The pathogenesis of acute pulmonary edema associated with hypertension

Gandhi, Sanjay; Powers, John C.; Nomeir, Abdel-Mohsen

doi:10.1016/s1062-1458(01)00228-8

Cited by 89 publications

(114 citation statements)

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“…However, our focus was on the pathophysiological explanation for an elevated EDP at rest and resultant pulmonary edema, which has been observed in several investigations. 11,49,50 The data at the 16-and 20-week time points suggest that extracardiac factors, specifically renal dysfunction, play an important pathophysiological role in the genesis of this clinical aspect of this syndrome.…”

Section: Discussionmentioning

confidence: 99%

“…Heart failure with a normal or preserved EF in the setting of hypertension is a heterogeneous clinical syndrome with various associated comorbid conditions 47 and a spectrum of clinical presentations ranging from effort or exercise intolerance 48 to elevated LV EDP with 49 or without 50 acute pulmonary edema. Recent studies have demonstrated that increased ventricular vascular stiffening 3,11,42 characterized by upward and leftward shifted ESPVR and EDPVR (eg, at the 12-week time period in the HS rats) can result in increased load lability 11 and is closely correlated with exercise duration and peak oxygen consumption.…”

Section: Discussionmentioning

confidence: 99%

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Development of Heart Failure in Chronic Hypertensive Dahl Rats

et al. 2006

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Abstract-The impact of hypertension on left ventricular (LV) structure, pump function, and heart failure in Dahl salt-sensitive rats is poorly characterized but hypothesized to yield insights into the pathophysiology of heart failure with normal or preserved ejection fraction. Eighty Dahl salt-sensitive rats were fed either a high-salt (HS) or low-salt (LS, controls) diet starting at age 7 weeks. Ventricular properties were measured by echocardiography, hemodynamics and end-systolic and end-diastolic pressure-volume relationships (ESPVR and EDPVR, respectively). Compared with LS controls, HS rats developed severe hypertension and LV hypertrophy. At week 12, HS rats developed passive diastolic dysfunction (leftward/upward shifted EDPVR, increased chamber stiffness) with reductions in end-diastolic volume. However, the ESPVR also shifted upward (enhanced end-systolic function) so that overall pump function was enhanced compared with LS, and there was no change in end-diastolic pressure (EDP). At 16 and 20 weeks, HS hearts enlarged so that end-diastolic volumes and EDPVRs became similar to the respective age-matched LS controls. Concomitantly, the ESPVRs and overall pump function curves also moved toward controls, and ejection fraction declined. Despite normal or enhanced overall pump function at these times, EDP and wet lung weight increased, indicative of development of heart failure. In the Dahl salt-sensitive rat, which pathophysiologically retains salt and water, the development of heart failure (increased EDP and wet lung weight) is dissociated from changes in passive diastolic and active systolic properties. These observations suggest that a volume overload sate plays an important pathophysiological role in development of heart failure despite preserved overall ventricular pump function in this model of chronic hypertension. Key Words: remodeling Ⅲ heart failure Ⅲ diastole Ⅲ hypertrophy Ⅲ renal disease H eart failure commonly occurs in patients with a normal or preserved ejection fraction (HFPEF). 1-3 It was advocated previously that HFPEF is primarily because of diastolic dysfunction and, thus, termed "diastolic heart failure" (DHF). 4,5 However, data from our recent clinical and animal studies suggest that HFPEF can occur without diastolic dysfunction. 6 -10 We found that HFPEF in the setting of idiopathic hypertrophic cardiomyopathy and infiltrative cardiac diseases is indeed because of diastolic dysfunction, defined by a reduced chamber capacitance in the absence of systolic dysfunction. 10 However, in the setting of long standing hypertension, HFPEF may not always be because of diastolic dysfunction. 10 We proposed other, extracardiac factors leading to a volume-overloaded state as the underlying pathology, such as might occur with salt and water handling impairments encountered in the setting of renal dysfunction.Two potential limitations of prior studies contribute to the controversy. First, barring a few notable exceptions, 7,11-13 studies of HFPEF have evaluated diastolic properties without any ser...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Development of Heart Failure in Chronic Hypertensive Dahl Rats

et al. 2006

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“…However, in hypertensive patients, HF may be because of either LV systolic or diastolic dysfunction. 18 Previous reports established that HF with normal EF is common in hypertensive patients, particularly at old age, 19,20 and most studies in humans with diastolic HF reported normal LV volumes. 21 When challenged by hemodynamic stress, the LV of hypertensive patients is unable to increase the EDV (ie, it has limited preload reserve) because of decreased LV relaxation and compliance.…”

Section: Perspectivesmentioning

confidence: 99%

Heart Failure and Left Ventricular Remodeling After Reperfused Acute Myocardial Infarction in Patients With Hypertension

et al. 2006

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Abstract-In the thrombolytic era, hypertension has been shown to adversely affect the development of heart failure after acute myocardial infarction (AMI). We sought to examine the relation between antecedent hypertension and heart failure after mechanical reperfusion and to test the impact of postinfarction left ventricular remodeling on heart failure in hypertensive patients. A series of 953 patients (324 hypertensives) with AMI treated with successful primary percutaneous coronary intervention underwent a 5-year follow-up. A subgroup of 325 subjects underwent 2D echocardiography at admission, 1 month, and 6 months. From day 1 to 6 months, despite similar improvement in regional and global left ventricular function and similar 6-month infarct artery patency rate, left ventricular end-diastolic volume increased in the normotensives (122Ϯ36 mL to 131Ϯ47 mL; PϽ0.001) but not in the hypertensives (127Ϯ41 mL to 128Ϯ31 mL; Pϭ0.768). At 6 months, the incidence of left ventricular remodeling in hypertensive and normotensive patients was not different (22% versus 28%; Pϭ0.210). However, at 5 years, the incidences of hospitalization for heart failure (7% versus 3%; Pϭ0.014) and of New York Heart Association functional class Ն2 (53% versus 40%; PϽ0.001) were higher in hypertensive as compared with normotensive patients. Hypertension was found to be a predictor of heart failure (hazard ratio, 2.23; Pϭ0.015). In conclusion, patients with antecedent hypertension are at higher risk to develop heart failure after AMI, even when successfully reperfused by primary percutaneous coronary intervention. However, the increased incidence of heart failure in hypertensive patients is not associated with a greater propensity to postinfarction left ventricular remodeling. Key Words: heart failure Ⅲ hypertrophy Ⅲ remodeling Ⅲ coronary artery disease Ⅲ myocardial infarction H ypertension is a well-known risk factor for coronary artery disease and heart failure. It has been shown that after thrombolysis for acute myocardial infarction (AMI), antecedent hypertension increases the risk of heart failure (HF) and other adverse events. [1][2][3][4][5] The progression to HF after AMI is mainly related to left ventricular (LV) remodeling. 6 However, animal 7,8 and human studies 5,9,10 evaluating the relation between hypertension and early LV remodeling after AMI have yielded conflicting or inconclusive results.Several studies have demonstrated that mechanical reperfusion (primary percutaneous coronary intervention, PCI) is superior to pharmacological reperfusion (thrombolysis), because it allows brisk and sustained flow achievement in the infarct-related artery (IRA) in a higher proportion of patients with subsequent improved myocardial salvage and better long-term outcome. 11 Thus, in the last decade, an increasing number of centers have adopted primary PCI as the preferred reperfusion therapy for AMI.In this study, we sought to examine the relation between antecedent hypertension and the development of HF after successful primary PCI for AMI. An...

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“…These main hemodynamic alterations expose the lung vasculature to pressure-induced challenges whose most immediate acute threat is pulmonary edema. 4 In the long term, the sustained backward hemodynamic transmission, along with the potential contribution of mitral insufficiency, increases the pulsatile loading on the right ventricle (RV) 5 and triggers pulmonary hypertension (PH) development and symptom exacerbation. 6 Thus, as a consequence of hemodynamic and functional perturbations, PH-HFpEF develops as a more advanced corollary of diastolic HF, leading to abnormal phenotypes of the lung microcirculation, 7,8 the arterial system, and right heart function 9-11 ( Figure 1).…”

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confidence: 99%