Echocardiographic alterations in patients with non-functioning adrenal incidentaloma.

OBJECTIVE: While left ventricular (LV) dysfunction has been described in patients with Cushing's syndrome (CS), data concerning morphologic and functional cardiac alterations in patients with incidentally discovered adrenal masses [adrenal "incidentaloma" (AI)], without overt hypercortisolism, are lacking. In this study the echocardiographic characteristics of patients with AI were evaluated and then compared with those of lean and obese normotensive subjects. SUBJECTS AND METHODS: Twenty-one patients with AI, without clinical or subclinical hypercortisolism, 18 normotensive obese subjects matched for gender and body mass index (BMI) and 20 normotensive lean subjects were studied. Echocardiography was performed in all subjects. In all patients plasma ACTH, serum cortisol, and DHEA-S levels were measured. RESULTS: Patients with AI showed greater impairment of several echocardiographic indices of LV hypertrophy and diastolic dysfunction compared to normotensive lean subjects (p<0.05), but did not differ from those in obese subjects. Hypertensive AI patients showed a greater alteration of echocardiographic parameters (p<0.05) and higher BMI (p<0.01) and cortisol values (p<0.05) than normotensive ones. Plasma ACTH and serum cortisol were similar in AI patients and in obese controls, while DHEA-S levels were lower in AI (p<0.05). No correlations between cortisol secretion and echocardiographic parameters were found. CONCLUSION: In patients with non-functioning AI there is an impairment of cardiac morphology and function. These data suggest that patients with AI should be carefully screened also by means of echocardiographic studies.

Functional ischemic mitral regurgitation in anterior ventricular remodeling: results of surgical ventricular restoration with and without mitral repair.

Ischemic functional mitral regurgitation following ischemic cardiomyopathy is a secondary phenomenon to ventricular dilation, and therapeutic approaches to this complication are not uniform. Solutions to improve mitral function include either mitral repair or observing the effects of coronary revascularization and/or ventricular rebuilding during surgical ventricular restoration (SVR). The present study of 108 patients (comprising 18% of our 588 SVR population) reports the effects of mitral repair following SVR and CABG by comparing geometric, functional, hemodynamic and outcome changes to SVR patients without mitral repair. The degree of mitral regurgitation went from 2.9 +/- 1.2 before to 0.7 +/- 0.7 after SVR and mitral repair. SVR improved EF from 29 +/- 7% to 34 +/- 10% p 0.001; reduced end diastolic volume from 243 +/- 74 to 163 +/- 53 ml and end systolic volume from 170 +/- 63 to 107 +/- 41 ml, p 0.000. Ventricular size and shape geometric measurements improved in all patients, either with and without mitral repair. SVR improved tenting and papillary muscle width between muscle heads in all patients, but alterations in mitral annular size improved only following mitral repair. Preoperative mitral regurgitation occurred in patients with larger ventricular volume and lower ejection fraction and was an independent predictor of operative mortality risk.

Surgical treatment of ventricular septal defect complicating acute myocardial infarction. Experience of a north Italian referral hospital.

The purpose of our study was to evaluate the clinical outcome of postinfarction ventricular septal defect (VSD) of patients referred to our institution for surgical treatment, by assessing the role of several operative, pre- and post-operative variables on mortality. The medical records of 58 consecutive patients (mean age 73+/-7 years), operated on after 14+/-12 days from the acute myocardial infarction were retrospectively reviewed and the data were analyzed. Associated procedures were left ventricular reconstruction in 13 patients and aortocoronary bypass grafting in 47 (81%). The overall operative, in-hospital mortality rate was 52% (75% in patients operated on within the first week and 16% if time from infarct to surgery was >3 weeks). Time from AMI to surgery and time from hospital admission to operation were significantly shorter in non-survivors (p=0.003 and 0.012, respectively). Other pre-operative variables significantly associated with mortality were: cardiogenic shock, pulmonary pressure, VSD diameter. In conclusion, time from AMI to operation appears to be a very important prognostic factor. However, size of VSD and hemodynamic conditions significantly influence the mortality. Moreover, concomitant procedures of revascularization can be safely performed, when required, as actually occurs in most cases.

Variable response to atrial pacing after intravenous propranolol in patients with stable exertional angina.

The effect of propranolol administration on regional coronary haemodynamics were investigated in 14 patients with stable exertional angina and isolated left anterior descending artery disease. Thermodilution was used to measure great cardiac vein flow (GCVF) and anterior regional coronary resistance (ARCR) under control conditions, at peak atrial pacing, after i.v. propranolol administration (0.1 mg kg-1) and at the peak of repeated atrial pacing. Propranolol did not change peak pacing heart rate, systolic blood pressure or double product. Peak pacing GCVF decreased slightly but non-significantly after drug administration from 84 +/- 20 to 79 +/- 24 ml min-1, while ARCR increased, but again non-significantly, from 1.36 +/- 0.44 to 1.45 +/- 0.45. Analysis of individual patient responses revealed that propranolol prolonged peak pacing time and hence peak pacing heart rate (from 126 +/- 24 to 140 +/- 23 beats min-1, P less than 0.05) in five patients. In such patients, peak pacing systolic blood pressure was lower than the pre-propranolol atrial pacing (145 +/- 35 vs 165 +/- 33, P less than 0.001) so that double product remained unchanged. Moreover, peak pacing ARCR did not change after propranolol (pre-propranolol 1.47 +/- 0.46, after propranolol 1.40 +/- 0.56 mmHg.ml-1.min, P = ns) while it increased significantly in the nine patients who did not improve after the drug (before propranolol 1.30 +/- 0.44, after propranolol 1.48 +/- 0.41 mmHg.ml-1.min, P less than 0.02). These data suggest that the response to atrial pacing after i.v. propranolol administration is variable as some patients tolerate higher heart rates while others do not.(ABSTRACT TRUNCATED AT 250 WORDS)

Comparison of the effectiveness of dihydroquinidine and quinidine on ventricular ectopy after acute and chronic administration.

The aim of this study was to compare the pharmacokinetics and antiarrhythmic activity of dihydroquinidine and quinidine in 14 patients (11 men, 3 women, aged 28 to 67 years) with heart disease and chronic, stable, high-frequency premature ventricular beats (PVB) (greater than 100/hr). A randomized, double-blind, crossover, placebo-controlled protocol was utilized. During Holter monitoring the patients were given either dihydroquinidine or quinidine as the gluconates in an oral solution (600 mg); blood samples were taken 0.5, 1, 1.5, 2, 4, 6, 8, and 12 hours later. The patients were then assigned to three successive treatment periods of 7 days each: dihydroquinidine HCl (900 mg/day), quinidine polygalacturonate (1,650 mg/day), or placebo. At the end of each period 24-hour Holter monitoring was carried out and a blood sample was taken for determination of drug concentration. By comparing the area under the curves dihydroquinidine was 59% as available as quinidine; rates of absorption and elimination were similar. Mean peak blood levels of dihydroquinidine and quinidine were 1.06 +/- 0.34 and 2.15 +/- 0.96 micrograms/ml, respectively. After dihydroquinidine, eight patients had a positive response (greater than 50% reduction in PVB frequency), while seven patients responded to quinidine. During maintenance treatment both dihydroquinidine (233 +/- 330) and quinidine (234 +/- 311) reduced the mean PVB frequency per hour compared to placebo (690 +/- 569). Nine patients (64%) on dihydroquinidine and eight (57%) on quinidine had greater than 70% decrease in mean PVB frequency per hour. Steady-state peak plasma concentrations of dihydroquinidine and quinidine were 1.10 +/- 0.41 and 2.24 +/- 1.13 micrograms/ml, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)