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Differences in generalist and specialist physicians' knowledge and use of angiotensin-converting enzyme inhibitors for congestive heart failure.

OBJECTIVE: To quantify the extent and determinants of underutilization of angiotensin-converting enzyme (ACE) inhibitors for patients with congestive heart failure, especially with respect to physician specialty and clinical indication. DESIGN: Survey of a national systematic sample of physicians. PARTICIPANTS: Five hundred family practitioners, 500 general internists, and 500 cardiologists. MEASUREMENTS AND MAIN RESULTS: Physicians' choice of medications were determined for four hypothetical patients with left ventricular systolic dysfunction: (1) new-onset, symptomatic; (2) asymptomatic; (3) chronic heart failure, on digitalis and diuretic; and (4) asymptomatic, post-myocardial infarction. For each patient, randomized controlled trials have demonstrated that ACE inhibitors decrease mortality or the progression of symptoms. Among the 727 eligible physicians returning surveys (adjusted response rate 58%), approximately 90% used ACE inhibitors for patients with chronic heart failure who were already taking digitalis and a diuretic. However, family practitioners and general internists chose ACE inhibitors less frequently (p < or = .01) than cardiologists for the other indications. Respective rates of ACE inhibitor use for each simulated patient were new-onset, symptomatic (family practitioners 72%, general internists 76%, cardiologists 86%); asymptomatic (family practitioners 68%, general internists 78%, cardiologists 93%): and asymptomatic, postmyocardial infarction (family practitioners 58%, general internists 70%, cardiologists 94%). Compared with generalists, cardiologists were more likely [p < or = .05] to increase ACE inhibitors to a target dosage (45% vs 26%) and to tolerate systolic blood pressures of 90 mm Hg or less [43% vs 15%). CONCLUSIONS: Compared with cardiologists, family practitioners and general internists probably underutilize ACE inhibitors, particularly among patients with decreased ejection fraction who are either asymptomatic or post-myocardial infarction. Educational efforts should focus on these indications and emphasise the dosages demonstrated to lower mortality and morbidity in the trials.

Adult↗

Importance of two-dimensional echocardiographic assessment of left ventricular systolic function in patients presenting to the emergency room with cardiac-related symptoms.

BACKGROUND: This prospective study was designed to test the hypothesis that the assessment of left ventricular systolic function at the time of emergency room (ER) presentation provides valuable diagnostic and prognostic information in patients with cardiac-related symptoms. METHODS AND RESULTS: The study is based on a 2-year follow-up of 171 consecutive patients evaluated in the ER for such symptoms. In the course of follow-up, one third of the patients (55 of 171) suffered a major cardiac event. For those with left ventricular systolic dysfunction (LVSD), the age-adjusted rate of early events (occurring within 48 hours of presentation) was more than eight times higher than for those without LVSD (26.9% versus 3.3%, p less than 0.01). For events occurring after 48 hours of ER presentation, LVSD was associated with a nearly fourfold excess of cardiac events (23.9% versus 6.4%, p less than 0.01). Other than advanced age, the most important confounder for early events included an abnormal electrocardiogram diagnostic for acute myocardial infarction. Confounders for late events included advanced age and a history of hypertension. LVSD on two-dimensional echocardiography (2DE) was the only finding associated with early and late events after controlling for other risk factors. In addition, the prediction of these events derived from the combination of historical, clinical, electrocardiographic, and 2DE findings was significantly improved when accounting for the presence or absence of LVSD (p less than 0.01). CONCLUSIONS: We conclude that the 2DE assessment of left ventricular systolic function provides valuable diagnostic and prognostic information in subjects presenting to the ER with cardiac-related symptoms.

Angina Pectoris↗

Triphasic mitral inflow velocity with mid-diastolic flow: the presence of mid-diastolic mitral annular velocity indicates advanced diastolic dysfunction.

Mitral inflow filling pattern usually consists of 2 forward flow velocities in sinus rhythm: early rapid filling (E) and late filling with atrial contraction (A). However, additional mid-diastolic flow velocity may be present resulting in triphasic mitral inflow filling pattern. When mitral inflow is triphasic, mitral annulus velocity recorded by tissue Doppler imaging (TDI) frequently demonstrates a mid-diastolic component (L'). The significance of L' has not been explored previously. The purpose of this study was to explore possible mechanisms and clinical implications of triphasic mitral inflow with or without L' using TDI and proBNP. Of 9004 patients who underwent transthoracic echocardiography from March to November 2003, 83 (0.9%) patients (33 male, 50 female; mean age, 63+/-10 years) with a triphasic mitral inflow velocity pattern, including mid-diastolic flow velocity of at least 0.2m/s, and sinus rhythm were prospectively identified in our clinical echocardiography laboratory. Peak velocity of E, mid-diastolic (L), and A, and deceleration time (DT) of the E wave velocity were measured. Diastolic mitral annular velocities were measured at the septal corner of the mitral annulus by TDI from the apical 4-chamber view. ProBNP was measured at the time of echocardiogram using a quantitative electrochemiluminescence immunoassay. Mean heart rate was 54+/-6 beats/min (range, 40-67). Mean left ventricular (LV) ejection fraction (EF) was 64+/-13% and LV systolic dysfunction (EF<40%) was present in only 6 (7%). Patients were classified into 2 groups: group 1 (n=47) included those who had L' and group 2 (n=36) included those without L'. Group 1 patients had significantly higher peak velocity (35+/-14 vs 26+/-6 cm/s, p=0.0002) and TVI (35+/-14 vs 26+/-6 cm/s, p=0.0002) of L, E/E' (18+/-8 vs 14+/-6, p=0.02), and left atrial volume index (42+/-14 vs 34+/-10 ml/m(2), p=0.0037). E' (4.7+/-1.3 vs 6.2+/-2.3 cm/s, p=0.001) and A' (6.2+/-2.0 vs 8.6+/-3.4 cm/s, p=0.0006) were significantly lower in group 1 compared with those of group 2. ProBNP was significantly higher in group 1 (847+/-1461 vs 438+/-1039 pmol/l, p=0.0012) and it was above normal in all except in 1 patient of group 1. In conclusion, the presence of L' in subjects with triphasic mitral inflow velocity pattern with mid-diastolic flow is associated with higher E/E', elevated proBNP and enlarged left atrium indicating advanced diastolic dysfunction with elevated filling pressures. This unique mitral annular velocity pattern should be helpful in identifying the patients with advanced diastolic dysfunction and increased LV filling pressures.

Adult↗

Functional valvular incompetence in decompensated heart failure: noninvasive monitoring and response to medical management.

OBJECTIVE: We hypothesized that functional mitral and tricuspid valvular incompetence (MR and TR, respectively) are reversible causes of reduced cardiac output in decompensated heart failure (DF) that accompanies systolic dysfunction in ischemic or nonischemic cardiomyopathy. BACKGROUND: DF, defined as signs and symptoms of heart failure at rest, is rooted in a salt-avid state transduced by neurohormonal activation secondary to impaired renal perfusion. Functional MR and TR are reversible causes of reduced systemic blood flow. Their impact on cardiac output, thoracic fluid content, cardiac chamber dimensions, and valvular apparatus function can be monitored noninvasively, before and after optimized medical management. METHODS: Fourteen male subjects (66 +/- 8 years old) with reduced ejection fraction (24 +/- 5%) secondary to ischemic (71%) or nonischemic (29%) cardiomyopathy, who developed DF with clinical evidence of mitral (MR) and tricuspid (TR) valvular incompetence, were each assessed by bioimpedance and echocardiography before and 1 week after optimized medical management restored compensated failure. RESULTS: Pharmacologic elimination of DF was accompanied by a reduction in body weight (P < 0.01). Hemodynamic improvements included a rise in cardiac index (2.1 to 2.6 L/min/m2; P < 0.01) and a reduction in predicted pulmonary artery systolic pressure (58 to 35 mm Hg; P < 0.001), thoracic fluid content (39 to 32 kOhm; P < 0.001), and systemic vascular resistance (1633 to 1209 dynes/sec/cm5; P < 0.001). Improvements in functional MR and TR included reductions in left and right atrial areas (27 to 24 cm and 26 to 23 cm2, respectively; P < 0.001), color-flow grading of MR and TR severity (P < 0.01), mitral regurgitant volume (105 to 65 mL; P < 0.001), and effective MR orifice size (0.8 to 0.6 cm2; P < 0.01). CONCLUSIONS: In DF, functional MR and TR contribute to reduced cardiac output, increased thoracic fluid content, and systemic vascular resistance, together with enlarged atria and valvular orifice size, which can be improved by medical management. Bioimpedance and echocardiography provide for serial noninvasive assessments of hemodynamic status and valvular function in such cases.

Aged↗

[Characteristics and course of patients over 65 years of age with severe heart failure].

INTRODUCTION AND OBJECTIVES: Although there have been many studies on the prognosis of congestive heart failure, most of them have not provided specific data about older patients. The aim of our study is to evaluate general characteristics and short and medium-term evolution of patients older than 65 years with severe heart failure. PATIENTS AND METHODS: We have carried out a prospective study of all patients older than 65 years admitted to our Department during 1993 due to severe heart failure (functional class III or IV of the NYHA classification), regardless of the etiology. In that year, 84 patients who fulfilled those criteria were admitted. RESULTS: The mean age was 72 +/- 6 years, 56% were male and 44% female. Age distribution was as follows: 36 patients were between 65 and 70 years, 27 between 70 and 75, 8 between 75 and 80, and 13 older than 80. The etiology of heart failure was: ischemic heart disease 44%, valvular heart disease 36%, idiopathic dilated cardiomyopathy 8%, systemic arterial hypertension 7% and other etiologies 5%. Significant systolic dysfunction (left ventricular ejection fraction < 0.45) was present in 36% of the patients. Ten percent of the patients suffered from severe ventricular arrhythmias (ventricular tachycardia or fibrillation). Regarding treatment, 24% underwent valvular surgery, 74% received only medical treatment and coronary angioplasty was performed in one patient. In hospital mortality was 9% (8 patients). After a mean follow-up of 8 +/- 4 months, the probability of survival was 78% at 1 month, 71% at 6 months and 63% at 1 year. The survival rate was better in patients with higher ejection fraction (53% for patients with ejection fractions of less than 0.45, 64% for those with ejection fractions between 0.45 and 0.60 and 79% for those with ejection fractions greater than 0.60). Considering etiology, the survival rate was worse for patients with acute myocardial infarction (30%) and aortic valve stenosis (58%). CONCLUSIONS: Patients older than 65 years admitted to the hospital for severe congestive heart failure represent a heterogeneous population in respect to etiology, systolic function and prognosis. Nevertheless, from this study it appears that a worse prognosis was associated with the lower left ventricular ejection fractions and with certain etiologies; such as acute myocardial infarction or aortic stenosis.

Age Factors↗

[Hemodynamic and electrophysiologic changes in hypertrophic cardiomyopathy].

Hypertrophic cardiomyopathy is characterized by abnormalities of the myocardium, and the activation and conduction tissues, that may have separate manifestations, but often occur together in complex clinical pictures. The subaortic gradient, although not always present, is the most classical manifestation of the disease, with its typical dynamic behavior, changing with preload, afterload and contractility. In most cases it is due to systolic motion of the mitral valve against the septum in systole, but in a few it is caused by midventricular "constriction". Alteration of diastolic ventricular function is important, and probably the main cause of heart failure, that is usually accompanied by normal systolic function. Mitral insufficiency is common in the obstructive forms, due to the abnormal mitral valve motion, but in some cases it may be due to structural abnormalities of the valve. There may be systolic constriction, or nonatherosclerotic occlusion of the intramyocardial coronary arteries, causing myocardial infarction and ventricular aneurysms, that may lead to systolic dysfunction. The electrocardiogram is rarely normal. Hypertrophy patterns, deeply inverted T waves, deep Q waves, QRS slurring suggestive of WPW syndrome without true preexcitation are the most common manifestations. Rhythm disturbances are common and include sinus node dysfunction, superconductor atrioventricular node or heart block. Atrial fibrillation is frequent and may have catastrophic consequences, including systemic embolism. Non-sustained ventricular arrhythmias are often present, but its predictive value for sudden death is unclear. Monomorphic ventricular tachycardia is infrequent, and programmed stimulation is more likely to precipitate polymorphic ventricular tachycardia of difficult clinical interpretation. Sudden death may be due to multiple mechanisms, and it is difficult to predict and prevent.

Arrhythmias, Cardiac↗

Mitral reconstruction in cardiomyopathy.

Functional mitral regurgitation (MR) is a significant complication of end-stage cardiomyopathy, and may affect most heart failure patients as a pre-terminal or terminal event as it develops secondary to a change in the annular-ventricular apparatus and altered ventricular geometry; this results in incomplete leaflet coaptation.. Historically, surgery in MR patients was mitral valve replacement, but the adverse effects on LV systolic function of interrupting annulus-papillary muscle continuity was poorly understood. At the University of Michigan (1993-2000), 140 patients with end-stage cardiomyopathy and refractory MR underwent mitral valve repair with an undersized flexible annuloplasty ring. All were in NYHA class III/IV despite receiving maximal medical therapy, and had severe LV systolic dysfunction (ejection fraction (EF) <25%). Overall operative mortality was 5%. There were five 30-day mortalities (one intraoperative death due to right ventricular failure, one cardiac failure, one stroke, two multisystem organ failure). Five patients required intra-aortic balloon pump IABP support, but no patients required a LV assist device. Mean follow up was 38 months (range: 1-68 months); one- and two-year actuarial survival was 80% and 70%, respectively. There were 26 late deaths. At postoperative echocardiography the mean transmitral gradient was 3 +/- 1 mmHg (range: 2-6 mmHg). At two-year follow up, all patients were in NYHA class I/II, with mean EF 26%. NYHA class was improved in all patients, and all reported subjective improvement in functional status. Improvements were shown in LV EF, cardiac output, and end-diastolic volumes, with reduced sphericity index and regurgitant fraction. Though significant undersizing of the mitral annulus was used to over-correct for the zone of coaptation, no mitral stenosis was induced, nor was any systolic anterior motion (SAM) noted. SAM was avoided due to widening of the aortomitral angle and increased LV size seen in myopathic patients. In conclusion, surgical therapies of heart failure are rapidly expanding and evolving. As a result of improvements in preoperative selection, intraoperative techniques and postoperative care, high mortality and morbidity after surgical intervention in patients with end-stage heart disease no longer apply. By combining operative techniques with optimal medical management of heart failure, good outcome can avoid or postpone transplantation. This strategy will help to preserve the limited number of donor organs for those patients with no other surgical or medical alternatives.

Cardiomyopathies↗

[Improvement of the pre-hypertensive inherited cardiac dearangements with phenylalanine in essential hypertension].

OBJECTIVE: To assess whether phenylalanine intervention can effectively improve the pre-hypertensive inherited cardiac hypertrophy and systolic dysfunction in young offsprings of patients with essential hypertension (ER). METHODS: Ninty-six normotensive adolescents with hypertensive family history and associated with inherited cardiac hypertrophy, i.e, interventricular, septum (IVST) and (or) left ventricular post wall thickness (PWT) > or = 10.5 mm, were screened according to the normal range criteria of ultrasonic-cardiogram (UCG) obtained previously from 50 normotensive adolescents without hypertensive genetic predisposition. The UCG parameters before and after 3, 6, 9 months of observation were compared between intervention group (Phe 1 g/d 58 subjects) and placebo-control group (placebo 1 g/d, 38 subjects) in 2 separate trials by a double-blind, randomized, cross-over and comparable placebo-control design. RESULTS: The hypertrophy and dilatation of ascending aorta and left heart structure were regressed after intervention, i.g, the changes after 9 months intervention, IVST dropped from 10.9 +/- 1.2 to 9.2 +/- 0.6 mm, PWT from 9.5 +/- 1.0 to 8.6 +/- 0.6 mm, left ventricular mass index from 92 +/- 15 to 70 +/- 11 g/m2; All of the parameters reflecting the systolic function of left ventricle were improved in pooled group of 2 trials. The UCGs after placebo was fundamentally not changed except some sporadic values. The results were similar in 2 separate trials. The improvement after Phe and its return towards that of pre-intervention after stope were remarked at 6 months. CONCLUSION: The inherited cardiac dearrangement seen in adolescents with hypertensive genetic predisposition can be assumed to be the pre-hypertensive changes of EH. It can be reversed by phenylalanine--a natural and essential amino-acid.

Adolescent↗

B-type natriuretic peptide in the diagnosis and management of congestive heart failure.

Finding a simple blood test that would aid in the diagnosis and management of patients with CHF clearly would have a favorable impact on the staggering costs associated with the disease. BNP, which is synthesized in the cardiac ventricles and correlates with LV pressure, amount of dyspnea, and the state of neurohormonal modulation, makes this peptide the first potential "white count" for heart failure. The fact that a point-of-care rapid assay for BNP has been approved by the FDA gives the clinician an opportunity to explore its potential usefulness. The author's data, and data from others, suggest that serial point-of-care testing of BNP will be of immense help in patients presenting to urgent care clinics with dyspnea. Additionally, BNP might serve as a screen for patients referred for echocardiography. A low BNP level makes echocardiographic indices of LV dysfunction (systolic and diastolic) highly unlikely. BNP also might be an effective way to improve the in-hospital management of patients admitted with decompensated CHF. In some instances, BNP levels may obviate the need for invasive hemodynamic monitoring and, in cases where such monitoring is used, may help tailor treatment of the decompensated patient. Finally, the role of BNP in the outpatient cardiac or primary care clinic may be one of critical importance in titration of therapies and in assessment of the state of neurohormonal compensation of the patient.

Atrial Natriuretic Factor↗

Right and left ventricular area and function determined by two-dimensional echocardiography in adults with the Eisenmenger syndrome from a variety of congenital anomalies.

The Eisenmenger syndrome has been associated with right ventricular (RV) enlargement and systolic dysfunction. However, little attention has been directed toward potentially characteristic changes in left ventricular (LV) dimensions or function. Therefore, 2-dimensional echocardiography (short-axis-papillary muscle level) was performed in 24 adults (mean age 33 +/- 7 years) with Eisenmenger syndrome to evaluate RV and LV size and function. A significant correlation was found between RV and LV end-diastolic areas (r = 0.96; regression slope 1.06), and fractional area change (r = 0.88; regression slope 1.03) in patients with a nonrestrictive ventricular septal defect (VSD) (n = 15). In contrast, in patients with Eisenmenger syndrome but no VSD (n = 9), RV and LV end-diastolic areas (r = 0.68; regression slope 0.10), and fractional area change (r = 0.08; regression slope -0.09) were discordant. RV function was preserved in most patients with a VSD, and mean RV fractional area change was significantly greater than in those without a VSD (0.50 +/- 0.13 vs 0.18 +/- 0.08; p < 0.001). No significant difference was apparent in these 2 groups (patients with and without a VSD) with respect to age, pulmonary artery systolic pressure, partial arterial oxygen pressure or hematocrit. Thus, the results indicate a relation between biventricular chamber dimensions and systolic function that is dependent on the nature and locus of the primary intracardiac defect responsible for the Eisenmenger syndrome.

Adult↗

Left ventricular filling pattern in uncomplicated obesity.

To determine if uncomplicated obesity is associated with systolic dysfunction or impairment of left ventricular (LV) filling, 40 normotensive, white, asymptomatic, obese subjects (16 men and 24 women, mean +/- SD age 35 +/- 13 years; body mass index 36 +/- 6 kg/m2) and 40 normotensive, normal-weight, white volunteers matched for age and sex distribution, were studied by Doppler echocardiography. Endocardial and midwall shortening did not show differences between groups (obese = 33 +/- 4% and 17 +/- 2%; normal weight = 33 +/- 3% and 18 +/- 2%, respectively). LV mass index was higher in obese than in normal-weight subjects (p <0.0001). Obese persons had prolonged isovolumic relaxation time (p <0.0001), lower transmitral peak early diastolic filling wave (E) velocity (p <0.02), higher E velocity deceleration time (p <0.002) and lower E/atrial diastolic filling wave (A) flow velocity ratio (p <0.01) than did normal-weight subjects, even after controlling for age and blood pressure. Between-group differences in E and E velocity deceleration time disappeared when controlling for LV mass index, whereas prolonged isovolumic relaxation time in obesity was independent of LV mass, chamber dimension, and end-systolic stress. LV filling variables were not statistically related to endocardial or midwall shortening, both as absolute value or as a percentage of that predicted from wall stress. We conclude that uncomplicated obesity is associated with primary impairment of LV isovolumic relaxation; abnormalities of early passive filling flow in obesity are associated with increased LV mass.

Adult↗

Reduction of N terminal-pro-brain (B-type) natriuretic peptide levels with exercise-based cardiac rehabilitation in patients with left ventricular dysfunction after myocardial infarction.

INTRODUCTION: N-terminal-pro-brain (B-type) natriuretic peptide (NT-pro-BNP) is a peptide hormone released from ventricles in response to myocyte stretch. The aim of the study was to investigate the influence of exercise training on plasma NT-pro-BNP to verify if this parameter could be used as a biological marker of left ventricular remodelling in myocardial infarction patients undergoing an exercise training programme. METHODS: Forty-four patients after myocardial infarction were enrolled into a cardiac rehabilitation programme, and were randomized in two groups of 22 patients each. Group A patients followed a 3-month exercise training programme, while group B patients received only routine recommendations. All patients underwent NT-pro-BNP assay, and cardiopulmonary exercise test before hospital discharge and after 3 months. RESULTS: In Group A, exercise training reduced NT-pro-BNP levels (from 1498+/-438 to 470+/-375 pg/ml, P=0.0026), increased maximal (VO2peak+4.3+/-2.9 ml/kg per min, P<0.001; Powermax+38+/-7, P<0.001) exercise parameters and work efficiency (Powermax/VO2peak+1.3+/-0.4 Power/ml per kg per min, P<0.001); there was also an inverse correlation between changes in NT-pro-BNP levels and in VO2peak (r=-0.72, P<0.001), E-wave (r=-0.51, P<0.001) and E/A ratio (r=0.59, P<0.001). In group B, at 3 months, no changes were observed in NT-pro-BNP levels, exercise and echocardiographic parameters. CONCLUSION: Three months exercise training in patients with moderate left ventricular systolic dysfunction after myocardial infarction induced a reduction in NT-pro-BNP levels, an improvement of exercise capacity and early left ventricular diastolic filling, without negative left ventricular remodelling. Whether the reduction of NT-pro-BNP levels could be useful as a surrogate marker of favourable left ventricular remodelling at a later follow-up remains to be further explored.

Biomarkers↗

[Diastolic filling of the right ventricle in patients with arterial hypertension and ischemic heart disease].

Our objective in this study was to compare particular features of pathogenesis of diastolic dysfunction of the right ventricle (RV) in patients with arterial hypertension (AH), stable exertional angina, and myocardial infarction of the left ventricle (LV) and to establish diagnostic significance thereof. As many as 429 AH patients presenting with different clinical forms of ischemic heart disease (IHD) were examined. Of these, 209 patients presented with stage I to III AH, 105 had functional class (FC) I-III stable exercise-induced angina, 115 patients had acute LF myocardial infarction (MI) verified by clinical findings, changes in ECG, and time-course of activity of myocardial enzymes. The control group was 30 essentially healthy subjects with no signs of cardiovascular and respiratory affections. All examinees underwent Doppler echocardiography as recommended by the American Society of Echocardiography. Measured in the above series were LV wall relative thickness, LV ejection fraction (EF) as recommended by L. Teichholz et al., LV isovolumetric relaxation time (IVRT), peak velocities of early (E) and atrial (A) filling of the heart's ventricles, E/A ratio, early diastolic filling deceleration time (DT) for both transmitral and transtricuspid flows, acceleration time of systolic flow in the pulmonary trunc as an indirect indicator of pressure in it. In AH patients, there was a close direct correlation between indices for filling of both ventricles (E/A ratio, E-wave DT and IVRT) but no significant correlation between indices for RV diastolic function and dimensions of left chambers or LV EF. In AH patients, disturbances in the diastolic function of the heart were at their greatest in eccentric hypertrophy of the myocardium when in the presence of pseudonomal and restrictive indices for LV filling "pseudonormalization" of the transtricuspid flow was being formed. In stable angina and MI, it was LV systolic dysfunction and pulmonary diastolic dysfunction that proved to play a major part in the development of RV diastolic dysfunction, its indices correlating significantly with heart failure and stable angina functional classes.

Angina Pectoris↗

Contrast-enhanced magnetic resonance and thallium scintigraphy in the detection of myocardial viability: a prospective comparative study.

The aim of the present study was to prospectively compare contrast-enhanced magnetic resonance imaging (CE-MRI) with single-photon emission tomography using (201)Thallium chloride (SPECT Tl) in the detection of myocardial viability. Patients with chronic coronary artery disease and systolic dysfunction defined by an ejection fraction (EF) <or= 45% were included. CE-MRI was performed 10-15 minutes after the administration of a gadolinium-based contrast agent using an Inversion Recovery Turbo FLASH (fast low-angle shot) sequence. A 4-hour rest redistribution protocol was used for SPECT Tl. Radionuclide ventriculography was used for the assessment of EF. Forty patients with an EF of 33.1 +/- 7.7% were included. Thirty-two underwent a follow-up examination after revascularization. Comparison of viability assessment was performed in 1360 segments. Agreement was noted in 1065 (78.3%) segments, resulting in a kappa value of 0.336. Discrepancies were observed in 96 SPECT Tl viable segments that were described as nonviable according to CE-MRI and in 199 SPECT Tl nonviable segments that were viable in the CE-MRI study. In patients undergoing the follow-up examination, EF increased by 5.5 +/- 7.3% (33.6 +/- 8.6% to 39.2 +/- 9.7%), but the relation between the amount of dysfunctional viable myocardium defined by both methods studied and the change in EF after revascularization was very weak and not statistically significant. Moderate agreement in the myocardial viability assessment between CE-MRI and SPECT Tl was observed. CE-MRI seems to be more accurate in identifying myocardial viability in inferior and inferolateral segments. We were unable to verify if either of the methods studied is useful for the prediction of EF improvement after revascularization.

Contrast Media↗

Ultrafiltration and dry weight-what are the cardiovascular effects?

Long-term prognosis in dialysis is poor compared to that in healthy control persons. A worsening of the prognosis is noted especially for patients who at initiation of dialysis have congestive heart failure, ischemic heart disease, or left ventricular dysfunction or hypertrophy. This is the main reason that cardiovascular causes are the most common for morbidity in these patients. The weight obtained when normal urine output is present is the dry weight. With reduced ability to excrete the volume by the kidneys in end-stage renal disease (ESRD), the body will retain water and the patient will gain weight. This extra weight is due to volume overload. While volume overload may induce a rise in blood pressure, if the heart is in acceptable condition, a fast removal of fluid by ultrafiltration (UF) during dialysis may instead cause hypotension. Ultrafiltration failure in peritoneal dialysis (PD) patients may lead to successive water retention and overhydration with subsequent cardiac failure, while volume overload may occur over a few days in hemodialysis (HD) patients. Anemia or even too-high hematocrit may impair cardiac function further and worsen conditions caused by wrong dry weight. Thus, during long-term and sustained volume overload, left ventricular (LV) hypertrophy will occur in an eccentric manner. A sustained overload then may lead to cell death and LV dilatation and, eventually, systolic dysfunction. Once a severe left ventricular dilatation has developed, the blood pressure may decrease during volume overload. A worsened prognosis is seen if malnutrition and low albumin levels are present. Volume overload necessitates ultrafiltration to achieve dry weight. Thereby, volume contraction contributes to exaggerated stimulation of or response to activation of the RAS and alpha-adrenergic sympathetic systems. If ultrafiltration goes beyond these compensatory mechanisms, hypotension will occur and increase the risk for hypoperfusion of vital organs. Such episodes may cause cardiac morbidity, aspiration pneumonia, vascular access closure, or neurological complications (seizures, cerebral infarction), besides a more rapid lowering of residual renal function. Preventive measures are, first, finding the right dry weight; second, minimizing interdialytic weight gain; third, optimizing the target for hemoglobin (110-120 g/l); fourth, lowering dialysate calcium (1.25 mmol/l); and fifth, eventually using higher dialysate potassium if long dialyses are performed.

Body Water↗

Electrocardiographic changes suggestive of myocardial ischemia elicited by dipyridamole infusion in acute rejection early after heart transplantation.

Acute cardiac rejection, syndrome X, and arterial hypertension can induce small vessel damage and, therefore, restriction of coronary reserve in the presence of normal epicardial coronary arteries. A characteristic response pattern to dipyridamole (DIP) infusion has been previously described in syndrome X and arterial hypertension: ST segment depression without any measurable systolic dysfunction. The aim of this study was to establish whether acute cardiac rejection might induce electrocardiographic alterations during DIP infusion. Changes in the 12-lead electrocardiogram and two-dimensional echocardiogram during high-dose DIP infusion (up to 0.84 mg/kg in 10 minutes) were evaluated within 24 hours of endomyocardial biopsy in 14 transplanted patients. A total of 47 biopsy-controlled DIP studies were performed within 5 weeks after cardiac transplantation. For each patient, at least 7 days elapsed between two consecutive studies. Electrocardiographic and echocardiographic tracings were analyzed without prior knowledge of endomyocardial biopsy findings. No remarkable side effects occurred in any case, so that the DIP study could be completed in all patients. A diagnostic (greater than 0.1 mV) ST segment depression was found in 11 studies. The sensitivity and specificity of DIP-induced ST segment depression for the detection of biopsy-proven acute rejection were 72% and 94%, respectively. These data show that DIP stress is feasible and safe in transplanted patients and that acute cardiac rejection can be accompanied by DIP-induced ST segment depression without detectable impairment in systolic function. These changes might provide noninvasive markers for surveillance of rejection.

Adult↗

Lethal outcomes in patients with symptomatic heart failure developed after Q-wave myocardial infarction.

The article analyses clinical characteristics and mortality of patients with symptomatic chronic heart failure following Q-wave myocardial infarction. During the study 224 patients (mean age 64.1+/-9.7) with symptomatic chronic heart failure and left ventricular ejection fraction <40% were followed-up for 1-5 years (on the average, 2.6+/-2.0 years). The majority of the studied patients had had anterior or anterior-lower Q-wave myocardial infarction (61.6% and 25.9%, respectively) and an identified Canadian function class II-IV angina pectoris (74.6%), and one-fifth of the patients (19.6%) had unstable angina pectoris. All patients were diagnosed with chronic heart failure New York Heart Association function class II-IV, the majority of patients had disturbances in cardiac rhythm and conduction, almost a half of them (46.0%) had left ventricular aneurysm, 92.8% of patients were diagnosed with marked changes in left ventricular geometry, 84.4% of patients had II-IV degrees mitral regurgitation, a half of the patients had significant left ventricular diastolic dysfunction, and 6.3% of patients had previously experienced thromboembolic complications. During the follow-up period 132 patients died. The comparison of the characteristics of patients who survived with those of patients who died showed that the deceased patients were statistically significantly older compared to survivors; in addition to that, marked stenoses of three coronary arteries, severe chronic heart failure, ejection fraction < or =20%, ventricular extrasystoles, and sinal tachycardia were more common in the former group, and patients who died less frequently were overweight and less frequently used beta adrenoblockers. The evaluation of Kaplan-Meier curves showed that total mortality resulting from the development of chronic heart failure symptoms and indications of chronic heart failure during the 1st year was 21.0%, during the 2nd year -40%, during the 3rd year -55.0%, during the 4th year -61.0%, and during the 5th year -65.0% the highest mortality was observed when left ventricular ejection fraction < or =20%, and age >75. The development of severe chronic heart failure resulted, on the average, after 1.5+/-1.1 years. It is obvious that symptomatic chronic heart failure caused by ischemic cardiomyopathy and marked left ventricular systolic dysfunction following Q-wave myocardial infarction is a rapidly progressing process conditioning high risk of lethal outcome within the period of several years.

Adult↗

Connective tissue and the heart. Functional significance and regulatory mechanisms.

The heart has a three-dimensional extracellular fibrillar collagen scaffolding that normally serves a variety of functions important to tissue integrity and efficiency of muscular systolic pump and diastolic suction pump function (see article by Kovács). An adverse accumulation of extracellular matrix structural protein compromises tissue stiffness and adversely affects myocardial viscoelasticity, this leads to ventricular diastolic and systolic dysfunction. Hormonal factors, such as chronic, inappropriate (relative to dietary salt intake and intravascular volume) elevations in circulating angiotensin II and aldosterone, are accompanied by fibrosis of right and left sides of the heart. Hemodynamic factors regulate cardiac myocyte work and their adaptive hypertrophic growth. The relative contributions of hormonal and hemodynamic factors in regulating growth of muscular and nonmuscular compartments must form the basis for the selection of pharmacologic intervention that will optimize the management of symptomatic heart failure that accompanies hypertensive heart disease and ischemic cardiomyopathy. Cardioprotective strategies that prevent alteration of normal cardiac tissue structure by fibrosis and appearance of abnormal ventricular stiffness (viscoelasticity) are based on negating the generation of these hormones or interfering with their receptor-ligand binding. A regression of established cardiac fibrosis and improvement in abnormal ventricular stiffness is feasible. Experimental and clinical findings with lisinopril in hypertensive heart disease, where cardiac fibrosis and abnormal ventricular stiffness are present, indicate that such cardioreparation should be a targeted objective of pharmacologic intervention. Systematic analysis of this approach using a controlled clinical trial format is warranted. In recognizing the importance of viscoelastic elements in regulating the mechanical behavior of cardiac tissue, and in turn systolic and diastolic ventricular function, a broader tissue compartment based paradigm (ECM versus myocyte) for the management of heart failure emerges.

Collagen↗