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Only few studies aimed at identifying predictors of heart failure (HF) in hypertrophic cardiomyopathy (HC) patients. Furthermore, serial echocardiographic analyses are lacking in these patients and little is known about the natural progression of left ventricular (LV) abnormalities and their association with HF development. Aim of this study was to assess the prognostic value of LV global longitudinal strain (GLS) and other clinical and echocardiographic characteristics for the development of HF in patients with nonobstructive HC; furthermore, changes in echocardiographic parameters over time were correlated with HF development. Echocardiography was performed in 236 HC patients (68% men, age: 50 ± 14 years) at their initial visit and during follow-up (6.5(4.1 to 9.8) years). The end point of new HF development or progression to New York Heart Association class III/IV was noted and echocardiographic changes over time were compared among patients with and without HF using linear mixed model analysis. In total, 40 patients reached the HF end point. Multivariable cox regression analysis showed that age (HR 1.04(1.01 to 1.06), p = 0.016), New York Heart Association class (HR 2.30(1.07 to 4.95), p = 0.033), GLS (HR 1.15(1.05 to 1.22), p = 0.001), and left atrial volume (LAVI, HR 2.22(1.10 to 4.50), p = 0.027) were independently associated with the HF end point. Echocardiographic parameters, including GLS and LAVI, remained stable over time in patients without HF end point, but changed significantly in patients who developed HF (group-time interaction, p = 0.042 for GLS and p = 0.027 for LAVI). In conclusion, LV dysfunction is a progressive phenomenon in nonobstructive HC patients which can be detected by repeated echocardiography. Importantly, GLS and LAVI at baseline as well as their changes over time are associated with HF.

We evaluated whether long-term cardiac resynchronization therapy affects the inducibility of ventricular tachyarrhythmias in relation to reverse remodeling in cardiac arrest survivors with either ischemic or idiopathic dilated cardiomyopathy. Clinical, electrophysiologic, and echocardiographic data of 18 patients were obtained before and after 6 months of cardiac resynchronization.

Survivors of cardiac arrest due to ventricular arrhythmias are at risk for recurrent events. The role of revascularization in secondary prevention for survivors of cardiac arrest has been addressed in various studies with conflicting results. A total of 142 survivors of cardiac arrest with coronary artery disease were evaluated according to a standardized protocol, including 2-dimensional echocardiography, myocardial perfusion scintigraphy, coronary angiography, and electrophysiologic testing. Revascularization of scintigraphically documented ischemic myocardial regions was performed in 44 patients (31%). Final therapy was based on the results of electrophysiologic testing. Four-year survival rates were 100% for revascularized noninducible patients, 84% for revascularized inducible patients, 91% for nonrevascularized noninducible patients, and 72% for nonrevascularized inducible patients. Only 1 patient (

We evaluated whether cardiac resynchronization therapy affects the prevalence of ventricular tachycardia in relation to reverse remodeling in patients with end-stage heart failure. Clinical, echocardiographic, and implantable cardioverter-defibrillator (ICD) data of 17 patients with ICDs were obtained before and after they had received an upgrade to an ICD-cardiac resynchronization therapy device.

angiotensin-converting enzyme inhibitor therapy on 30-day outcome in patients 65 years of age with chronic congestive heart failure. Am J Cardiol 2000;86: 1151–1153. 2. Philbin EF, Rosso TA Jr, Lindenmuth NW, Ulrich K, Jenkins PL. Systolic versus diastolic heart failure in community practice: clinical features, outcomes and the use of angiotensin-converting enzyme inhibitors. Am J Med 2000;109: 605–613. 3. Aronow WS, Kronzon I. Effect of enalapril on congestive heart failure treated with diuretics in elderly patients with prior myocardial infarction and normal left ventricular ejection fraction. Am J Cardiol 1993;71:602–604. 4. Warner JG Jr, Metzger DC, Kitzman DW, Wesley DJ, Little WC. Losartan improves exercise tolerance in patients with diastolic dysfunction and a hypertensive response to exercise. J Am Coll Cardiol 1999;33:1567–1572. 5. Aronow WS, Ahn C, Kronzon I. Effect of propranolol vs no propranolol on total mortality plus nonfatal myocardial infarction in older patients with prior myocardial infarction, congestive heart failure, and left ventricular ejection fraction 40% treated with diuretics plus angiotensin-converting enzyme inhibitors. Am J Cardiol 1997;80:207–209. 6. Vasan RS, Benjamin EJ, Levy D. Prevalence, clinical features and prognosis of diastolic heart failure: an epidemiologic perspective. J Am Coll Cardiol 1995;26:1565–1574. 7. Senni M, Redfield MM. Heart failure with preserved systolic function: a different natural history? J Am Coll Cardiol 2001;38:1277–1282. 8. Cohn JN, Johnson G. Heart failure with normal ejection fraction: the V-HeFT Study. Circulation 1990;81(supp III):III48–III53. 9. Ghali JK, Kadakia S, Bhatt A, Cooper R, Liao Y. Survival of heart failure patients with preserved versus impaired systolic function: the prognostic implication of blood pressure. Am Heart J 1992;123:993–997. 10. Aronow WS, Ahn C, Kronzon I. Prognosis of congestive heart failure after prior myocardial infarction in older men and women with abnormal versus normal left ventricular ejection fraction. Am J Cardiol 2000;85:1382–1384. 11. Senni M, Tribouilloy CM, Rodeheffer RJ, Jacobsen SJ, Evans JM, Bailey KR, Redfield MM. Congestive heart failure in the community: a study of all incident cases in Olmstead County, Minnesota, in 1991. Circulation 1998;98:2282–2289. 12. Vasan RS, Larson MG, Benjamin EF, Evans JC, Reiss CK, Levy D. Congestive heart failure in subjects with normal versus reduced left ventricular ejection fraction: prevalence and mortality in a population-based cohort. J Am Coll Cardiol 1999;33:1948–1955. 13. McDermott MM, Feinglass J, Lee PI, Mehta S, Schmitt B, Lefevre F, Gheorghiade M. Systolic function, readmission rates, and survival among consecutively hospitalized patients with congestive heart failure. Am Heart J 1997; 134:728–736. 14. Pernenkil R, Vinson JM, Shah AS, Beckham V, Wittenberg C, Rich MW. Course and prognosis in patients 70 years of age with congestive heart failure and normal versus abnormal left ventricular ejection fraction. Am J Cardiol 1997;79:216–219.

To compare the long-term efficacy and safety of sirolimus-eluting stents (SES) to those of bare-metal stents (BMS) for ST-segment elevation myocardial infarction, outcomes were assessed in 310 patients (mean age age 59 +/- 11 years, 78% men) included in the randomized MISSION! Intervention Study: A Prospective Randomised Controlled Trial to Evaluate the Efficacy of Drug-Eluting Stents Versus Bare-Metal Stents for the Treatment of Acute Myocardial Infarction after a median follow-up period of 38 months. All patients were treated with aspirin (lifelong) and clopidogrel for 1 year after stent implantation. Except for a significant difference between reference vessel diameters (SES 2.76 mm vs BMS 2.92 mm, p = 0.02), there were no significant differences in baseline and angiographic characteristics between the treatment groups (158 SES, 152 BMS). A significant difference between SES and BMS patients for all revascularization end points was found after the first year of follow-up. However, at 3 years of follow-up, although there was still a trend toward better clinical outcomes in SES-treated patients, differences were no longer significant (death 4.4% vs 6.6%, p = 0.41; target vessel related myocardial infarction 2.5% vs 4.6%, p = 0.32; target vessel revascularization 8.9% vs 15.8%, p = 0.06), target lesion revascularization 6.3% vs 12.5%, p = 0.06; and target vessel failure 12.0% vs 19.7%, p = 0.06). Three cases of very late (definite) stent thrombosis were observed in the SES group (1.9%) versus none in the BMS group (p = 0.14). In conclusion, the significant SES benefit (compared to BMS) in patients with ST-segment elevation myocardial infarctions at 1-year follow-up in terms of target vessel revascularizations decreased to some extent because of more similar target vessel revascularization rates during the 2 subsequent years. Rates of death and nonfatal recurrent MI remained comparable. (C) 2010 Elsevier Inc. All rights reserved. (Am J Cardiol 2010;106:4-12)

Orthostatic defense is commonly validated with a 60 ° to 80 ° head-up tilt test, addressing the step response rather than the response to permanent orthostasis. During the initial phase of tilt, neural factors predominate, while later, the slower humoral factors fade in. It has been demonstrated that, during adaptation of the circulatory system to the standing conditions, overshoot and undershoot occur. These oscillations hamper straight-forward interpretation of a tilt test, and may contribute to the inconclusiveness of current studies regarding the aging of orthostatic defense. Gradual, progressive, orthostatic load testing seems a valuable alternative. We used a novel, incremental, head-up tilt protocol (0 ° to 80 °, 13 increments) to impose graded orthostatic stress on 46 healthy young adult men (mean age ±SD 25 ± 3 years), ana on 16 healthy late middle-aged men (60 ± 4 years), while recording the electrocardiogram and the blood pressure. A first-order estimate of the heart rate range associated with the sympathovagal transition was made by combined analysis of heart rate and heart rate variability trends. We observed similar responses in heart rate, heart rate variability, and blood pressure. Supine heart rate (61 ± 8 vs 61 ± 7 beats/min), heart rate at the maximal tilt angle (86 ± 13 vs 84 ± 12 beats/min), sympathovagal transition (112 ± 82 vs 111 ± 76 beats/min), percent increase of the rate-pressure product (49 ± 23% vs 43 ± 20%), and the slope of the linear regression of the mean blood pressure on the sine of the tilt angle (8.7 ± 8.3 vs 9.2 ± 7.1 mm Hg) did not differ significantly. We conclude that aging, per se, does not impair orthostatic defense under gradually increasing orthostatic stress.

To identify the effect of myocardial ischemia on systemic neurohormones and vascular resistance, 32 untreated, normotensive patients with coronary artery disease underwent incremental atrial pacing until angina. Arterial and coronary venous lactate and arterial values of catecholamines and angiotensin II were determined at control, at maximal pacing rates, and at 1, 2, 5 and 30 minutes after pacing. Based on pacing-induced ST-segment depression (≥0.1 mV) or myocardial lactate production, or both, patients were selected as ischemic (n = 25) or nonischemic (n = 7). Baseline clinical and hemodynamic data were comparable. During pacing, chest pain was similar (20 ischemic vs 7 nonischemic patients). Also, hemodynamic measurements were comparable, except for contractility, which did not improve, and left ventricular end-diastolic pressure, which significantly increased in ischemic patients. Moreover, during ischemia arterial pressures increased significantly (13%) and systemic resistance increased from 1,470 ± 60 (control) to 1,632 ± 76 dynes · s · cm−5 5 minutes after pacing (p < 0.05) in ischemic but not in nonischemic patients. Pacing did not affect neurohormones in nonischemic patients. In contrast, norepinephrine in ischemic patients increased significantly from 1.7 ± 0.2 (control) to 2.6 ± 0.3 (maximal pacing) and to 3.0 ± 0.4 nmol/liter (1 minute after pacing), whereas angiotensin II levels increased from 6.2 ± 1.4 (control) to 9.3 ± 2.1 pmol/liter (1 minute after pacing, p < 0.05). Epinephrine only increased during maximal rates (0.9 ± 0.1 vs 0.6 ± 0.1 nmol/liter at control, p < 0.05). Thus, myocardial ischemia activates circulating catecholamines and angiotensin II, accompanied by systemic vasoconstriction. Because the latter may amplify ischemia, modulation of this neuroendocrine stimulation may be of therapeutic value.