lisinopril and Mitral-Valve-Insufficiency

Chronic mitral regurgitation imparts a volume load on the left atrium (LA). Because this chamber may dilate asymmetrically, changes in left atrial size may be underestimated using standard two-dimensional or M-mode techniques.. The effect of lisinopril therapy in the setting of chronic organic mitral regurgitation on LA dimension was studied using standard M-mode techniques and LA volumes using the biplane Simpson's method.. Mitral regurgitant fraction was reduced at one year in the lisinopril group versus the placebo group (-6.7%+/-3.5% versus 3.5%+/-3.2%, respectively; P<0.05). Significant reductions in both maximum and minimum LA volumes were seen in the lisinopril group (88+/-33 mL to 75+/-23 mL and 46+/-20 mL to 38+/-16 mL, respectively; P<0.01). This change in LA size was not appreciated when measurements were performed using standard M-mode techniques (from 44.3+/-6.9 mm to 44.1+/-7.4 mm; P=not significant). There was no significant relationship between change in LA volume and change in regurgitant fraction or systolic blood pressure. Change in LA volume was moderately correlated with change in left ventricular mass.. Angiotensin-converting enzyme inhibitor therapy reduces LA volume in the setting of chronic mitral regurgitation. This change in LA size is not apparent when standard M-mode techniques are used. Therefore, a volumetric assessment of atrial size in the setting of chronic mitral regurgitation proved to be superior to standard two-dimensional techniques.

Topics: Angiotensin-Converting Enzyme Inhibitors; Blood Pressure; Cardiac Volume; Chi-Square Distribution; Chronic Disease; Female; Heart Atria; Humans; Lisinopril; Male; Middle Aged; Mitral Valve Insufficiency; Observer Variation; Treatment Outcome

In long-term, 1-year follow-up, uptitration of angiotensin-converting enzyme inhibitor and nitrate therapy over established doses can further improve severe functional mitral regurgitation in patients with dilated cardiomyopathy due to a reversal of heart failure-related left ventricular remodeling. With marked left ventricular enlargement, >6.8 cm end-diastolic diameter, heart failure remodeling may be irreversible and resistant to further medical intervention.

Topics: Aged; Angiotensin-Converting Enzyme Inhibitors; Female; Heart Failure; Hemodynamics; Humans; Isosorbide Dinitrate; Lisinopril; Male; Middle Aged; Mitral Valve Insufficiency; Severity of Illness Index; Ultrasonography; Vasodilator Agents; Ventricular Remodeling

Angiotensin converting enzyme inhibitors (ACEIs) are widely used in the treatment of hypertension, myocardial infarction, and congestive heart failure. They have a known adverse effect of unresponsiveness to vasoconstrictors resulting in hypotension for the patients undergoing cardiac surgery. We report a case of a 43-year-old female patient with preoperative lisinopril (2.5 mg per day for a week prior to cardiac surgery), who was diagnosed with severe mitral and tricuspid valve regurgitation. She underwent both a mitral and tricuspid valve replacement operation using cardiopulmonary bypass (CPB). To address her ACEI-associated hypotension on cardiopulmonary bypass, bypass flows were as high as cardiac index of greater than 3 (3.1 +/- .2) L/min/m2 to provide sufficient perfusion indicated by cerebral oxymetry monitoring and adequate urine on pump. In addition, due to unresponsiveness to regular concentration of neosynephrine (neo), boluses of higher concentrations up to 320 microg/mL of neo were administered to maintain the perfusion pressure on pump. The patient was weaned from CPB uneventfully and was discharged home on postoperative day 7. Additional therapeutic treatment to ACEI-associated hypotension and unresponsiveness to neo for the patients undergoing cardiac surgery using CPB is reviewed as well in this paper.

Topics: Adult; Angiotensin-Converting Enzyme Inhibitors; Cardiopulmonary Bypass; Female; Humans; Hypotension; Lisinopril; Mitral Valve Insufficiency; Phenylephrine; Tricuspid Valve Insufficiency; Vasoconstrictor Agents

The goal of this study was to determine the therapeutic efficacy of angiotensin-converting enzyme (ACE) inhibitors and beta-adrenergic receptor blockers in experimental chronic mitral regurgitation (MR), gaining knowledge using methods difficult to apply in humans.. Both ACE inhibitors and beta-blockers are cornerstones in the treatment of human congestive heart failure. However, the roles of these treatments for chronic MR is unclear.. Mitral regurgitation was created in 11 closed-chest dogs. Three months after the creation, the ACE inhibitor lisinopril 20 mg was given orally daily. After three months of lisinopril therapy, the beta-blocker atenolol was added to lisinopril for another three months. Atenolol was begun at a dose of 12.5 mg daily and increased gradually to 100 mg daily. Hemodynamics and left ventricular (LV) function were assessed throughout the study.. Regurgitant fraction was consistently >50% over the course of this study. Pulmonary capillary wedge pressure and LV end-diastolic pressure were significantly increased after three months of MR and decreased during both lisinopril and the combined therapy in which it was not different from baseline. Left ventricular contractility measured by the end-systolic stiffness constant was depressed from 3.66 +/- 0.20 to 2.65 +/- 0.12 (p < 0.05) at three months of MR and rose insignificantly after lisinopril treatment (2.99 +/- 0.17). When atenolol was added, it rose significantly and returned to normal (3.50 +/- 0.22, p < 0.05).. Although lisinopril significantly reduced preload, its effect on LV contractility was insignificant in experimental MR. Conversely, atenolol, when added to lisinopril, achieved maximum hemodynamic benefit and also restored LV contractility.

Topics: Adrenergic beta-Antagonists; Angiotensin-Converting Enzyme Inhibitors; Animals; Atenolol; Dogs; Hemodynamics; Lisinopril; Male; Mitral Valve Insufficiency; Myocardial Contraction; Ventricular Function, Left

Topics: Aged; Angiotensin-Converting Enzyme Inhibitors; Atrial Fibrillation; Enalapril; Humans; Hypertension; Lisinopril; Lupus Erythematosus, Systemic; Male; Mitral Valve Insufficiency