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Echocardiographic Evaluation of Hypertensive Acute Pulmonary Edema

Echocardiographic Evaluation of Hypertensive Acute Pulmonary Edema

Status
Completed
Phases
Unknown
Study type
Observational
Source
ClinicalTrials.gov
Registry ID
NCT00829855
Enrollment
51
Registered
2009-01-27
Start date
2008-05-31
Completion date
2009-05-31
Last updated
2013-03-05

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Hypertension, Pulmonary Edema

Keywords

pulmonary edema, hypertension, echocardiography

Brief summary

Acute cardiogenic pulmonary edema (ACPE), one of the most severe forms of acute heart failure, represents 5% of hospital admissions. One of the most frequent phenomena encountered during ACPE is hypertensive crisis (hypertensive ACPE) but the mechanisms and causes of hypertensive ACPE are insufficiently understood. Few studies have evaluated the cardiac function during hypertensive ACPE, and these studies used only conventional echocardiography methods. New methods of evaluation of cardiac function in hypertensive ACPE (such as Tissue Doppler imaging) have not been used. The objectives of this study are to evaluate presence and role of the following potential mechanisms of hypertensive ACPE: 1. acute myocardial dysfunction (systolic and diastolic); 2. silent transient myocardial ischemia; 3. acute mechanical left ventricular dyssynchrony; 4. dynamic mitral regurgitation; 5. inter-ventricular interaction. Conventional and Tissue Doppler echocardiography will be used to assess cardiac function.

Interventions

None listed

Sponsors

Ministry of Education, Research, Youth and Sport, Romania
CollaboratorOTHER
Carol Davila University of Medicine and Pharmacy
Lead SponsorOTHER

Study design

Observational model
CASE_CROSSOVER
Time perspective
PROSPECTIVE

Eligibility

Sex/Gender
ALL
Age
18 Years to No maximum
Healthy volunteers
No

Inclusion criteria

* acute onset of dyspnea within the preceding 8 hours * respiratory distress and pulmonary rales at any level * pulmonary congestion confirmed by chest radiography * systolic blood pressure \> 160 mmHg before treatment * sinus rhythm * signed informed consent

Exclusion criteria

* acute myocardial infarction confirmed by myocardial necrosis markers (either CKMB or troponin I). Angina pectoris alone will not be excluded * significant left sided valvular disease (more than moderate). Mitral regurgitation of any severity will not be excluded, due to the hypothesis of the role of dynamic mitral regurgitation in the pathogenesis of acute hypertensive pulmonary edema * congenital heart disease * cardiac tamponade * rhythm and conduction disturbances that may have precipitated pulmonary edema, like sustained ventricular tachycardia and complete heart block

Design outcomes

Primary

MeasureTime frame
acute myocardial dysfunction (systolic and diastolic) and/or dyssynchronyacute event and 48 to 96 h after the event

Secondary

MeasureTime frame
surrogate markers of silent transient myocardial ischemiaacute event and 48 to 96 h after the event
dynamic mitral regurgitationacute event and 48 to 96 h after the event
inter-ventricular interactionacute event and 48 to 96h after the event

Countries

Romania

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Feb 4, 2026