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Background: In patients with acute heart failure (AHF), dyspnea relief is the most immediate goal. Renal dysfunction, diuretic resistance, and hyponatremia represent treatment impediments., Objectives: It was hypothesized that the addition of tolvaptan to a background diuretic improved dyspnea early in patients selected for an enhanced vasopressin antagonism response., Methods: In a double-blind trial, patients were randomized to tolvaptan 30 mg/day or placebo. Study entry required hospitalization within the previous 36 h, active dyspnea, and any of the following: 1) estimated glomerular filtration rate <60 ml/min/1.73 m 2 ; 2) hyponatremia; or 3) diuretic resistance (urine output ≤125 ml/h following intravenous furosemide ≥40 mg). The primary endpoint was a 7-point change in self-assessed dyspnea at 8 and 16 h, using a novel standardized approach., Results: We randomized 250 patients. There was no difference in the primary endpoint of day 1 dyspnea reduction, despite significantly greater weight reduction with tolvaptan (-2.4 ± 2.1 kg vs. -0.9 ± 1.8 kg; p < 0.001). At day 3, dyspnea reduction was greater with tolvaptan (p = 0.01). There were 2 significant treatment-by-subgroup interactions: patients without elevated jugular venous pressure and those without ascites showed directional favorability of tolvaptan over placebo for the primary endpoint compared with patients with these findings., Conclusions: Despite rapid and persistent weight loss with tolvaptan compared with placebo, in patients with AHF who were selected for greater potential benefit from vasopressin receptor inhibition, tolvaptan was not associated with greater early improvement in dyspnea. Apparent subsequent differences in dyspnea warrant further exploration of the temporal relationship between diuresis and dyspnea relief and a possible clinical role for tolvaptan. (Randomized, Double-Blind, Placebo Controlled Study of the Short Term Clinical Effects of Tolvaptan in Patients Hospitalized for Worsening Heart Failure With Challenging Volume Management [SECRET of CHF]; NCT01584557)., (Copyright © 2017 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Background: Slow oscillations (<1 Hz) during slow wave sleep (SWS) promote the consolidation of declarative memory. Children with attention-deficit/hyperactivity disorder (ADHD) have been shown to display deficits in sleep-dependent consolidation of declarative memory supposedly due to dysfunctional slow brain rhythms during SWS., Objective: Using transcranial oscillating direct current stimulation (toDCS) at 0.75 Hz, we investigated whether an externally triggered increase in slow oscillations during early SWS elevates memory performance in children with ADHD., Methods: 12 children with ADHD underwent a toDCS and a sham condition in a double-blind crossover study design conducted in a sleep laboratory. Memory was tested using a 2D object-location task. In addition, 12 healthy children performed the same memory task in their home environment., Results: Stimulation enhanced slow oscillation power in children with ADHD and boosted memory performance to the same level as in healthy children., Conclusion: These data indicate that increasing slow oscillation power during sleep by toDCS can alleviate declarative memory deficits in children with ADHD., (Copyright © 2014 The Authors. Published by Elsevier Inc. All rights reserved.)

Adjunctive balloon dilatation strategy has been shown to improve optimal stent deployment. As improvements in current stent designs evolve, less adjunctive balloon dilatation may be needed. However, few data currently exist to support this practice. We evaluated 88 native coronary lesions treated with single stent implantation (Nir, Tristar or S670). Serial intravascular ultrasound was performed after successful stent deployment and again after adjunctive balloon dilatation. To investigate further the precise expansion characteristics of the stents, serial volumetric intravascular ultrasound analyses were performed in 40 patients with automated pullback. After adjunctive balloon dilatation, minimal stent area increased significantly, from 6.4 +/- 2.1 to 7.4 +/- 2.2 mm(2) (p <0.001). Volumetric analysis showed a corresponding increase in stent volume index (6.6 +/- 1.8 to 7.5 +/- 2.0 mm(3)/mm, p <0.001). In the analysis of cross sections at 0.5-mm axial intervals, the percentage of cross sections, where stent area was > or =80% of the average reference lumen area, increased from 51% to 78% (p <0.001). Similarly, the percentage of cross sections, where stent area was > or =90% of the average reference lumen area, increased from 29% to 56% (p <0.001) with postdilatation. Postdeployment high- pressure balloon dilatation improved minimal stent area and volumetric expansion throughout the stented segment.

Ongoing advances in catheter-based technologies for the treatment of coronary artery disease have resulted in a steady increase in the volume of percutaneous coronary interventional procedures. This trend is likely to continue well into the next decade, and may be particularly pronounced among a high-risk population of patients. These high-risk patients, whether elderly, diabetic, presenting with preexisting renal insufficiency, congestive heart failure, prior bypass surgery, or diffuse atherosclerotic disease are at increased risk of renal compromise from contrast exposure and catheter manipulations within the aorta. Enhanced physician awareness of the renal implications of percutaneous coronary interventions, in conjunction with careful patient selection, risk assessment, and evolving renal protective strategies will help to minimize the incidence of renal complications and the associated increases in morbidity, mortality, and health care costs.

We describe the management of a patient, with a 13-year-old cadaveric renal transplant, who presented with acute myocardial infarction. Successful primary angioplasty was performed to the left anterior descending artery. It was complicated by transient renal failure and pseudoaneurysm of the femoral artery which was managed conservatively.

Four cases of papillary muscle rupture occurring in the setting of acute myocardial infarction are presented, which illustrate the following points: the diagnosis may not be apparent at presentation, a mitral regurgitant murmur may be absent, transesophageal echocardiography may establish the diagnosis when transthoracic echocardiography does not, and appropriate surgical correction can lead to excellent functional recovery.

Premature coronary artery disease is a late consequence of mediastinal radiation therapy. Many of these patients have been successfully treated with coronary bypass surgery. A 51-year-old man underwent bypass surgery for severe multivessel coronary disease 18 years following radiation therapy for a posterior mediastinal tumor. Recurrent angina 1 year later occurred following closure of the left internal thoracic artery graft. We suspect that this occurred as a consequence of injury sustained during mediastinal irradiation. Patients who have undergone prior mediastinal radiation therapy may not be assured the excellent long-term patency of the internal thoracic artery graft which has been reported for the general population. Saphenous vein grafts probably should be considered instead.

Combined nitrate/beta-blocker/nifedipine therapy is commonly used to treat refractory angina pectoris. We have observed "paradoxical" myocardial ischemia in ten patients with refractory angina (seven receiving combined beta-blocker and nitrate therapy, and three receiving nitrate treatment alone) in whom nifedipine (mean dosage, 92 mg/day; range, 60 to 120 mg/day) induced a decrease in blood pressure, angina pectoris (10/10 patients), and ischemic ECG changes (7/10 patients). These ten patients, all of whom regularly reported angina within 20 to 30 minutes of nifedipine ingestion, were prospectively studied before and after usual nifedipine dose administration, while blood pressures, heart rate, and ECGs were recorded. Mean systolic BP fell from 109 to 94 mm Hg after nifedipine (P less than .001, paired t test); mean heart rate increased from 64 to 68 beats per minute (P less than .05); seven patients developed transient ECG changes (five with ST-T wave depression and two with ST-T wave elevation) during the hypotensive period. Nifedipine may provoke angina and myocardial ischemia in certain patients with refractory angina pectoris receiving concomitant beta-blocker and nitrate therapy.

To determine the coronary anatomy responsible for electrocardiographic posterior myocardial infarction, the prevalence and severity of disease in the right coronary and left circumflex coronary arteries were compared in 21 patients with electrocardiographic posterior infarction (17 of whom had associated inferior infarction) and 23 patients with isolated electrocardiographic inferior infarction. Significant circumflex coronary artery disease (greater than or equal to 75% stenosis) was more prevalent in patients with posterior or inferoposterior infarction (17 of 21) than in those with isolated inferior infarction (11 of 23) (p less than 0.02). Significant right coronary artery disease was less prevalent in patients with posterior or inferoposterior infarction (16 of 21) than in those with isolated inferior infarction (23 of 23) (p less than 0.05). Among the 21 patients with posterior or inferoposterior infarction, disease was more severe in the circumflex coronary artery in 10 and the right coronary artery in 5 and was of equal severity in 6. Among the 23 patients with isolated inferior infarction, the more diseased artery was the right coronary artery in 21 and the circumflex artery in 2 (p less than 0.001 by chi-square analysis). Variant patterns of coronary artery dominance accounted for only 4 of the 17 patients with inferoposterior infarction. These data suggest that the likely substratum for electrocardiographic posterior or inferoposterior infarction is severe circumflex coronary artery disease, usually in association with significant right coronary artery disease. The pattern of tall, wide R waves in leads V1 or V2 (RV1,2) in patients with inferior infarction is highly predictive of at least two vessel coronary artery disease.

The unique association of both exercise-induced coronary arterial spasm and S-T segment depression with normal findings on selective coronary arteriography is described. The patient had a prior history of typical effort angina that had recently progressed to angina at rest. Despite the change in anginal pattern, the electrocardiogram disclosed S-T segment depression that was consistent with subendocardial ischemia, during both exercise testing and spontaneous chest pain. Exercise thallium-201 scintigraphy demonstrated the presence of large perfusion defects of the anterior and septal walls of the left ventricle. Coronary arteriographic findings, in the absence of symptoms, were entirely normal. Severe localized, reversible coronary spasm of the proximal left anterior descending coronary artery was subsequently demonstrated during spontaneous angina, isometric arm exercise and after the administration of ergonovine maleate. After treatment with isosorbide dinitrate and nifedipine, the patient had no further chest pain or electrocardiographic changes, and a repeated thallium-201 stress test revealed normal findings and greatly improved exercise tolerance.

A percutaneous approach via the brachial artery for coronary angioplasty is described. The technique employs a standard side arm sheath introducer system routinely intended for the femoral artery. Initial experience in ten cases shows this to be a relatively easy and safe alternative to conventional brachial arteriotomy, with some distinct advantages. It is less time consuming, permits the use of a variety of standard preformed guiding catheters, is associated with less patient discomfort, and the sheaths may be left in place for many hours if the angioplasty is complicated and/or long-term anticoagulation is desirable. Complications were limited to the female patients in this series. This technique is most suited to those operators who employ the brachial approach infrequently and only out of necessity in patients with severe peripheral vascular disease.

In 100 patients with coronary artery disease (CAD), the prevalence and severity of asynergy was determined for 9 left ventricular (LV) segments by both radionuclide and contrast angiography. The anterior, septal and lateral LV walls had significantly more prevalent and more severe asynergy in the medial segments than in the basal segments. In contrast, the inferior LV wall exhibited equally severe asynergy in both the medial and basal segments. In general, asynergy was most severe in the apical, medial septal, medial inferior and basal inferior LV segments. This asymmetric distribution of LV asynergy could not be explained by the distribution of occlusions or significant stenoses in the arterial tree, which were relatively uniformly distributed among the left anterior descending (32%), left circumflex (29%) and right (26%) coronary arteries. It is postulated instead that the asymmetric distribution of LV asynergy results from asymmetry of the coronary arterial tree supplying the left ventricle and that the prevalence of asynergy in an LV segment is directly related to its vascular distance from the coronary ostia. Unlike the relatively direct supply of the left anterior descending and circumflex arteries to the basal segments of the anterior, septal and lateral LV walls, the arterial supply to the basal inferior wall begins only after the right or dominant circumflex artery has traversed the length of the atrioventricular groove, significantly increasing its susceptibility to the pressure attenuation and occlusive jeopardy of more proximal stenoses.

The effect of incremental diltiazem dosing during concomitant digoxin administration over a four-week period in eight healthy adult volunteers (mean age, 28 +/- 4 years) was studied. The study group received 0.25 mg of digoxin twice daily for two days, after which they received 0.25 mg daily for the duration of the study. Following baseline electrocardiographic evaluation and measurement of trough digoxin levels, all subjects received 120 mg of diltiazem daily for one week, then 240 mg daily for one week, followed by 360 mg daily for one week. Resting electrocardiographic parameters (heart rate, P-R interval), renal function, electrolyte values, and digoxin and diltiazem concentrations were measured weekly. Daily administration of 360 mg of diltiazem plus 0.25 mg of digoxin resulted in a significant decrease in heart rate (from 68 +/- 9 beats per minute to 61 +/- 10 beats per minute; p less than 0.05), a marginal increase in P-R interval (from 169 +/- 22 msec to 179 +/- 21 msec; p = 0.08), and no significant change in trough serum digoxin concentration (from 0.85 +/- 0.08 ng/ml to 0.90 +/- 0.08 ng/ml; p = NS). The administration of up to 360 mg of diltiazem per day with 0.25 mg of digoxin per day was not associated with significant increases in serum digoxin concentrations in healthy subjects.

The relationship of personality factors to self-reported variations in symptoms of angina pectoris and their impact on functioning was examined in a sample of 50 cardiac patients. The frequency of anginal pains was significantly correlated with trait anger. The degree of perceived interference of angina with daily activities was related to Type A behaviour, anger and neuroticism. However, only neuroticism was related to the tendency to avoid activities because of the possibility of angina. Results are discussed in terms of the role of psychological factors in the manifestation and management of angina.

P2 300 selected patients, scalar electrocardiograms and contemporaneous radionuclide angiograms were analyzed retrospectively to assess the association between prominent right precordial R waves (duration greater than or equal to 0.04 second, R greater than or equal to S in lead V1 or V2), traditionally considered diagnostic of "posterior" infarction, and asynergy in various left ventricular segments. Mathematical methods for analysis of association between nonparametric variables clearly demonstrated that prominent right precordial R waves were strongly associated with asynergy of the basal lateral left ventricular wall, although asynergy of adjacent inferior and lateral segments was common. With the exclusion of right ventricular hypertrophy and bundle branch block, a prominent R wave in lead V1 exhibited a high specificity (greater than to 99%), a high positive predictive value (91%) and a low sensitivity (36%) for diagnosing basal lateral myocardial infarction. A prominent R wave in lead V2 exhibited a higher sensitivity (61%), a somewhat lower specificity (95%) and a significantly lower positive predictive value (76%). A newly developed criterion for such infarction--a prominent R wave in lead V2 and a Q wave inferior infarction--had intermediate characteristics and may be more clinically useful. The most common reasons for the decreased sensitivities of all three criteria were left ventricular hypertrophy or associated anterior myocardial infarction. These data demonstrate that prominent right precordial R waves are clinically useful in identifying inferior and lateral wall infarctions that involve the basal lateral left ventricular segment. Confusion results primarily from inappropriate use of the electrocardiographic term "posterior" for such infarctions.

Transient, acute severe aortic regurgitation documented by hemodynamic and Doppler-echocardiographic assessment was observed in an elderly woman immediately following balloon aortic valvuloplasty for critical aortic stenosis. Aortic regurgitation responded to medical therapy and resolved within 24 hr. Potential mechanisms are discussed. We suspect that an oversized balloon to aortic ring area stretched the annulus, separating the valve cusps and resulting in severe regurgitation, which rapidly normalized.

Right ventricular function was studied in 60 patients with equilibrium gated radionuclide angiography. The mean (+/- standard deviation) right ventricular ejection fraction in 20 normal subjects was 53 +/- 6 percent, a value in agreement with previous data from both radionuclide and contrast angiographic studies. This value was similar (55 +/- 7 percent) in 11 patients with coronary artery disease but normal left ventricular function. Radionuclide measurements of right ventricular ejection fraction were correlated with right heart hemodynamics. There was a significant negative linear correlation between right ventricular ejection fraction and mean pulmonary arterial pressure (r = -0.82) and between right ventricular ejection fraction and right ventricular end-diastolic pressure (4 = -0.67). Furthermore, patients with elevated right ventricular end-diastolic pressure and mean pulmonary arterial pressure had a more severely depressed ejection fraction than did those with an elevated mean pulmonary arterial pressure alone. Thus, an abnormal value for right ventricular ejection fraction by gated radionuclide angiography in the absence of primary right ventricular volume overload suggests abnormal right heart pressures, whereas a normal value excludes severe pulmonary arterial hypertension or an elevated right ventricular end-diastolic pressure.

Electrocardiographic ST-segment depression in the anterior precordial leads is a frequent observation during the initial hospital phase of acute transmural inferior myocardial infarction (MI), but is of uncertain significance. No available clinical studies have examined the prevalence of inferoseptal necrosis complicating inferior MI. Therefore, the clinical course, electrocardiographic features, radionuclide angiograms and cardiac enzyme changes in 57 patients with transmural inferior MI who did not have prior anterior or concomitant "true posterior" MI, associated anterior or posterolateral asynergy by radionuclide ventriculography, or left or right bundle branch block were reviewed retrospectively. Patients were categorized according to the presence (group A) or absence (group B) of precordial ST-segment depression and according to the presence (group I) or absence (group II) of radionuclide septal wall motion abnormalities. There were no significant differences in global left ventricular ejection fraction (group A, 49 +/- 8, group B, 52 +/- 41; group I, 51 +/- 7, group II, 51 +/- 6), right ventricular ejection fraction (group A, 45 +/- 9, group B, 42 +/- 7; group I, 43 +/- 8, group II, 41 +/- 8), or clinical outcome in the hospital. However, chi-square analysis revealed a significant (p less than 0.05) association between the presence or absence of septal asynergy and the presence or absence of precordial ST depression. In addition, average peak creatine kinase elevation (group I, 761 +/- 164 IU; group II, 698 +/- 178 IU) attained marginal significance by paired t test (p = 0.06). Precordial ST-segment depression during transmural inferior MI is frequently associated with septal asynergy by gated radionuclide angiography (15 of 26 patients, 58%).(ABSTRACT TRUNCATED AT 250 WORDS)

The relationship between scores on the Framingham Type A Scale (FTAS) and angiographic severity of coronary artery disease (CAD) was examined in a sample of 50 patients undergoing diagnostic cardiac catheterization. Age and family history of coronary heart disease (CHD) were positively related to CAD severity. Contrary to prediction, the FTAS demonstrated a non-significant, inverse relationship with CAD. However, FTAS-defined Type As with at least some CAD were younger than Type Bs with CAD. This inverse relationship between FTAS scores and age was not found in patients without CAD. Thus, though the FTAS was related to a younger clinical presentation requiring catheterization, it was not associated with the severity of CAD.