2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines

This review focuses on the systemic complications of acromegaly. Mortality in this disease is increased mostly because of cardiovascular and respiratory diseases, although currently neoplastic complications have been questioned as a relevant cause of increased risk of death. Biventricular hypertrophy, occurring independently of hypertension and metabolic complications, is the most frequent cardiac complication. Diastolic and systolic dysfunction develops along with disease duration; and other cardiac disorders, such as arrhythmias, valve disease, hypertension, atherosclerosis, and endothelial dysfunction, are also common in acromegaly. Control of acromegaly by surgery or pharmacotherapy, especially somatostatin analogs, improves cardiovascular morbidity. Respiratory disorders, sleep apnea, and ventilatory dysfunction are also important contributors in increasing mortality and are advantageously benefitted by controlling GH and IGF-I hypersecretion. An increased risk of colonic polyps, which more frequently recur in patients not controlled after treatment, has been reported by several independent investigations, although malignancies in other organs have also been described, but less convincingly than at the gastrointestinal level. Finally, the most important cause of morbidity and functional disability of the disease is arthropathy, which can be reversed at an initial stage, but not if the disease is left untreated for several years.

/pdf/systemic-complications-of-acromegaly-epidemiology-48hlt1tw8j.pdf

Systemic complications of acromegaly: epidemiology, pathogenesis, and management.

Preamble 2356

1. Introduction 2357

2. Overview of Acs 2358

3. Initial Evaluation and Management: Recommendations 2358

4. Early Hospital Care: Recommendations 2363

5. Myocardial Revascularization: Recommendations 2369

6. Late Hospital Care, Hospital Discharge, and Posthospital Discharge Care: Recommendations 2371

/pdf/2014-aha-acc-guideline-for-the-management-of-patients-with-z5d3l3bigd.pdf

2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes: Executive Summary

New Doppler echocardiographic applications for the study of diastolic function

Preamble e346

1. Introduction e347

2. Overview of Acs e349

3. Initial Evaluation and Management e350

4. Early Hospital Care e359

/pdf/2014-aha-acc-guideline-for-the-management-of-patients-with-1tcyxwwh37.pdf

2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes

SUMMARY Acromegaly isassociated with an increased cardiac morbidity andmortality, butitis notclear whether thisistheresult ofincreased incidence ofhypertension and coronary heart disease orofaspecific disease ofheart muscle. Thirty fouracromegalic patients were studied by non-invasive techniques. Sevenofthesepatients hadraised plasmaconcentrations ofgrowth hormone atthetimeofstudy; three were newlydiagnosed andhadnot received any treatment. Hypertension was presentinnine(26%)butonlythree(9%)hadelectrocardiographic left ventricular hypertrophy. Echocardiography showedventricular hypertrophy in12(48%)and increased left ventricular mass in17(68%)patients. Holtermonitoring detected important ventricular arrhythmias in14patients. Thallium-201 scanning showedevidence for coronary heart disease ineight patients. Systolic timeintervals were normal exceptwhenthere was coexistent ischaemic heart disease. A comparison between 19acromegalic patients withno otherdetectable causeofheart disease and22agematched controls showed appreciably abnormal left ventricular diastolic function inthegroupwithacromegaly. Theabnormalities showndidnotcorrelate with left ventricular mass orwallthickness. Therewas no difference indiastolic function between patients withactive acromegaly andthose withtreated acromegaly. Hypertensive acromegalic patients hadworsediastolic function thanhypertensive controls, suggesting that hypertension may further impair theleft ventricular diastolic abnormality inacromegaly. Thisisthefirst study tofind evidence ofsubclinical cardiac diastolic dysfunction inacromegaly anditsupports thesuggestion that there isaspecific disease ofheart muscle inacromegaly. Whilesystemic hypertension, atherosclerosis, and diabetes mellitus maycontribute- tocardiovascular complications inacromegaly, cardiac failure has occurred inpatients withacromegaly intheabsence ofthese andother established causes ofheart muscle disease.'" Suchcasessuggest theexistence ofa specific disease ofheart muscle inacromegaly. Postmortemstudies showed an"abnormal myocardium" in59%ofcases ofacromegaly and"definite myocarditis" in26%,' suggesting that cardiac dysfunction maybemorecommonthanclinical examination alone suggests. Although Jonas etalfound abnormal systolic timeintervals insixof10patients with

Subclinical cardiac dysfunction inacromegaly: evidence for aspecific disease ofheartmuscle

The appearance of impaired left ventricular diastolic function in chronic ischemic heart disease often precedes systolic dysfunction. Myocardial ischemia and increased calcium loading have been implicated in the genesis of increased left ventricular stiffness. We have assessed the effects of long-term therapy with different classes of calcium channel-blocking drugs on left ventricular peak filling rate in patients with chronic stable angina and congestive heart failure secondary to ischemic heart disease. Therapeutic effects of nicardipine (30 mg t.i.d.), nisoldipine (10 mg b.i.d.), and verapamil (120 mg t.i.d.) (4 weeks) have been assessed on radionuclide left ventricular diastolic filling parameters in patients with chronic stable angina using placebo-controlled studies. All three drugs significantly improved exercise capacity as compared with placebo. Verapamil produced significant improvements in peak filling rate (p less than 0.005), time to peak filling rate (p less than 0.01), and first one-third filling fraction (p less than 0.005), whereas nicardipine only improved peak filling rate (p less than 0.005); neither drug altered the mean ejection fraction (n = 20). Nisoldipine did not significantly alter diastolic filling parameters or ejection fraction (n = 10). Nisoldipine and digoxin were also assessed in congestive heart failure (New York Heart Association [NYHA] classes II and III) associated with ischemic heart disease (n = 26) (open parallel design). Neither produced significant alterations in peak filling rate and ejection fraction after 3 months of therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of long-term treatment with calcium antagonists on left ventricular diastolic function in stable angina and heart failure.

The effects of a new vasodilating β-blocking drug, carvedilol, were studied in 20 patients with chronic stable angina using a single-blind, placebo-controlled protocol. Two doses of carvedilol, 25 mg twice daily and 50 mg twice daily, were compared with placebo using analysis of variance. The study design consisted of 2 weekly phases of initial placebo followed by carvedilol, 25 mg twice daily and then 50 mg twice dally, and a second placebo period. Supine rest and exercise radionuclide ventriculography was performed at the end of each phase. Carvedilol produced a significant dose-related reduction in rest and exercise heart rate and blood pressure (p

Effects of a new vasodilating beta-blocking drug, carvedilol, on left ventricular function in stable angina pectoris.

Isosorbide 5-mononitrate (IS 5-MN) is an active metabolite of isosorbide dinitrate and is widely used as an antianginal agent. The acute and subacute (2 weeks) effects of IS 5-MN, 40 mg twice daily, were evaluated in 18 patients with stable angina pectoris using computerized exercise testing and a placebocontrolled, double-blind, randomized trial protocol. There were 2 phases of 2 weeks each in which patients received placebo or active IS 5-MN. Acute testing (8 patients) was performed 2 hours after the first dose and subacute testing 2 hours after the morning dose on day 14. Acute testing showed an increase in exercise time from a mean (± standard error of mean) of 8.2 ± 0.6 minutes to 11.1 ± 0.5 minutes (p

Acute and sustained effects of isosorbide 5-mononitrate in stable angina pectoris

The efficacy of carvedilol, a new vasodilating β -blocking drug, was evaluated in 20 patients with chronic angina using a single-blind, placebo-controlled protocol. A 2-week placebo phase was followed by therapy with carvedilol, 25 mg twice daily for 2 weeks, after which the dose was doubled. There was then a second placebo phase lasting 2 weeks. Treadmill exercise testing, 24-hour ambulatory electrocardiographic monitoring and drug blood level assays were performed at the end of each phase. Exercise time (mean ± standard error of mean) increased from 7.4 ± 0.5 minutes during placebo to 9.0 ± 0.5 minutes carvedilol, 25 mg twice daily (p 5 and CC 5 increased significantly, but peak ST depression did not change. Heart rate at rest was reduced at both dose levels, from 86 ± 4 beats/min during placebo to 70 ± 2 beats/min with 25 mg twice daily (p β -blocking drugs.

Antianginal efficacy of carvedilol, a beta-blocking drug with vasodilating activity.

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