Effect of growth hormone treatment on diastolic function in patients who have developed growth hormone deficiency after definitive treatment of acromegaly.

OBJECTIVE: Although growth hormone (GH) replacement is prescribed for patients with hypopituitarism due to many etiologies, it is not routinely prescribed for patients with GH deficiency (GHD) after cure of acromegaly (acroGHD). This study was designed to investigate the effect of GH replacement on cardiac parameters in acroGHD. DESIGN: We prospectively evaluated for 12months 23 patients with acroGHD: 15 subjects on GH replacement and eight subjects not on GH replacement. Main outcome measures included LV mass corrected for body surface area (LVM/BSA) and measures of diastolic dysfunction (E/A ratio and deceleration time), as assessed by echocardiography. RESULTS: After 12months of follow-up, there were no differences between the GH-treated group and the untreated group in LVM/BSA (GH: 74.4±22.5g/m(2) vs untreated: 72.9±21.3g/m(2), p=0.89), E/A ratio (GH: 1.21±0.39 vs untreated: 1.08±0.39, p=0.50) or deceleration time (GH: 224.5±60.1ms vs untreated: 260±79.8ms, p=0.32). The overall degree of diastolic function was similar between the groups with 42.9% of untreated subjects and 50% of GH-treated subjects (p=0.76) classified as having normal diastolic function at follow-up. CONCLUSIONS: There were no significant differences in LVM/BSA or parameters of diastolic function in patients with a history of acromegaly treated for GHD as compared to those who were untreated. These data are reassuring with respect to cardiovascular safety with GH use after treatment for acromegaly, although further longer term study is necessary to evaluate the safety and efficacy of GH treatment in this population.

Mitral valve and papillary muscle abnormalities in hypertrophic obstructive cardiomyopathy.

PURPOSE OF REVIEW: This section reviews abnormalities of the mitral valve apparatus that are associated with hypertrophic obstructive cardiomyopathy. RECENT FINDINGS: Mitral valve abnormalities in hypertrophic obstructive cardiomyopathy include leaflet elongation and thickening and hypertrophy with anterior displacement of the papillary muscles. This combination contributes to the development of systolic anterior motion. The resultant flow forces during systolic anterior motion pulling the leaflets into the left ventricular outflow tract also result in reduced leaflet coaptation and a posteriorly directed mitral regurgitant jet. Additional mitral valve abnormalities include degenerative leaflet changes, aberrant chordal attachments and papillary muscle anomalies. SUMMARY: Mitral valve abnormalities are common in hypertrophic obstructive cardiomyopathy and play an important role in the pathophysiology of dynamic left ventricular outflow tract obstruction.

Amiodarone-induced destructive thyroiditis associated with coronary artery vasospasm and recurrent ventricular fibrillation.

A 55-year-old male on long-term amiodarone therapy presented with ischaemic chest pain and recurrent unwitnessed syncope. Interrogation of his internal cardiac defibrillator, which had been inserted 4 years earlier, revealed two episodes of ventricular fibrillation, the timing of which corresponded to his syncopal events. Severe spontaneous coronary artery vasospasm was observed on coronary angiogram. Thyroid function testing revealed severe hyperthyroidism with a diagnosis of type 2 amiodarone-induced thyrotoxicosis (AIT) subsequently made. Treatment with prednisolone therapy was commenced and thyroid function rapidly normalized. Prednisolone was weaned without recurrence of hyperthyroidism and on last review, 6 months after initial presentation, he remains free from further chest pain and arrhythmias. Our patient's presentation is a very rare case of AIT-associated coronary artery spasm and documented ischaemic ventricular fibrillation with fortunate survival.

Left ventricular ejection fraction and absence of ACE inhibitor/angiotensin II receptor blocker predicts appropriate defibrillator therapy in the primary prevention population.

INTRODUCTION: Implantable cardioverter defibrillators (ICD) significantly reduce mortality in patients with left ventricular (LV) dysfunction. However, little is known of the predictors of appropriate device activation in the primary prevention population. The aim of the present study was to determine predictors of appropriate device therapy in patients receiving ICDs for primary prevention. METHODS & RESULTS: One hundred twenty-six patients with a left ventricular ejection fraction (LVEF) of < 35% and no prior documented ventricular arrhythmias underwent ICD implantation. The ICD implanted was single chamber in 60 (48%), dual chamber in 10 (8%), and biventricular in 56 (44%) patients and programmed with a single ventricular fibrillation (VF) zone at >180 beats per minute. Mean age was 58 +/- 13 years and mean LVEF was 23 +/- 7%. Fifty-two percent had ischemic cardiomyopathy and 66% were New York Heart Association heart failure class II/III. During a mean follow-up period of 589 +/- 353 days, 17 (13%) patients received appropriate device therapy and three (4%) received inappropriate shocks. Appropriate ICD therapy was associated with reduced LVEF (mean 19.9% vs 23.7%, P = 0.02) and the patients were less likely to have received angiotensin-converting enzyme inhibitor (ACEI) or angiotensin II receptor blockers (AIIRB) (65% vs 90%, P = 0.04). Multivariate analysis revealed lack of ACEI/AIIRB (odds ratio [OR]= 0.06, 95% confidence interval [CI]= 0.01-0.37, P = <0.01) and lower LVEF (OR = 0.88, 95% CI 0.79-0.98, P = 0.02) predicted appropriate device activation. There was no difference in transplant-free survival between the appropriate therapy and no/inappropriate therapy groups, LVEF <20% and LVEF >20% group, and lack of ACEI/AIIRB and ACEI/AIIRB group. CONCLUSION: Appropriate device activation occurred in 13% of patients in a primary prevention population. LVEF and absence of ACEI/AIIRB predicted appropriate ICD therapy.