Strain analysis reveals subtle systolic dysfunction in confirmed and suspected myocarditis with normal LVEF. A cardiac magnetic resonance study.

AIMS: Lake Louise Criteria (LLC) are time-dependent and some acute myocarditis (AM) with preserved left ventricular ejection fraction (LVEF) could be missed, due to the limited accessibility of Cardiac Magnetic Resonance (CMR). We aimed to assess the potential value of cardiac strain measured by feature tracking (FT) imaging in this population. METHODS AND RESULTS: Eighty-three patients with clinically suspected AM and normal LVEF were divided into 39 "confirmed AM" (positive LLC) and 44 "suspected AM" (negative LLC). An age and gender-matched sample of 42 normal subjects underwent CMR. In all groups, FT-derived biventricular strains and STE- global longitudinal strain (GLS) were assessed, being regularly measurable. Strain values < 5th percentile of the control group were considered abnormal. "Suspected" and "confirmed" AM were similar, except for medium time of CMR evaluation (5.2 vs 1 months from presentation, respectively; p = 0.004). Compared to healthy controls, both "suspected" and "confirmed" AM showed significantly impaired strain values. LV-global circumferential strain (GCS), right ventricular GCS and LV-GLS were abnormal in 15.4% and 15.9%, 20.5% and 15.9%, 7.7% and 9.1% in "confirmed" and "suspected" AM, respectively. STE analysis confirmed the results on LV-GLS, however a weak correlation emerged between STE and CMR-FT LV-GLS (p = 0.08). CONCLUSIONS: Compared to STE, CMR-FT analysis provided a more comprehensive and complementary biventricular strain evaluation that resulted similar in "confirmed" and "suspected" AM with normal LVEF. Conversely, mostly biventricular GCS was significantly reduced in up to 20% of patients, compared to healthy controls.

Non-alcoholic fatty liver disease is associated with left ventricular diastolic dysfunction in essential hypertension.

BACKGROUND AND AIM: Insulin resistance is recognized as the pathophysiological hallmark of non-alcoholic fatty liver disease (NAFLD). A relation between insulin sensitivity and left ventricular morphology and function has been reported in essential hypertension, where a high prevalence of NAFLD has been recently found. We investigated the inter-relationship between left ventricular morphology/function, metabolic parameters and NAFLD in 86 never-treated essential hypertensive patients subdivided in two subgroups according to the presence (n = 48) or absence (n = 38) of NAFLD at ultrasonography. METHODS AND RESULTS: The two groups were similar as to sex, age and blood pressure levels. No patient had diabetes mellitus, obesity, hyperlipidemia, or other risk factors for liver disease. Body mass index, waist circumference, triglycerides, glucose, insulin, homeostasis model of assessment index for insulin resistance (HOMA-IR), aspartate aminotransferase and alanine aminotransferase were higher and adiponectin levels were lower in patients with NAFLD than in patients without NAFLD, and were associated with NAFLD at univariate analysis. Patients with NAFLD had similar prevalence of left ventricular hypertrophy compared to patients without NAFLD, but a higher prevalence of diastolic dysfunction (62.5 vs 21.1%, P < 0.001), as defined by E/A ratio <1 and E-wave deceleration time >220 ms. Diastolic dysfunction (P = 0.040) and HOMA-IR (P = 0.012) remained independently associated with NAFLD at backward multivariate analysis. CONCLUSIONS: Non-alcoholic fatty liver disease was associated with insulin resistance and abnormalities of left ventricular diastolic function in a cohort of patients with essential hypertension, suggesting a concomitant increase of metabolic and cardiac risk in this condition.

Restrictive left ventricular filling pattern in dilated cardiomyopathy assessed by Doppler echocardiography: clinical, echocardiographic and hemodynamic correlations and prognostic implications. Heart Muscle Disease Study Group.

OBJECTIVES: This study was undertaken to evaluate the frequency of restrictive left ventricular filling pattern in dilated cardiomyopathy, as well as its clinical and hemodynamic correlations and prognostic implications. BACKGROUND: In dilated cardiomyopathy, as in other heart diseases, different left ventricular filling patterns were observed on Doppler echocardiography. Some patients showed a "restrictive filling pattern," similar to that associated with restrictive cardiomyopathy, characterized by predominant E waves and a shortened E deceleration time. METHODS: Pulsed Doppler transmitral curves were analyzed in 79 consecutive patients with dilated cardiomyopathy assigned to two study groups according to E deceleration time: group 1 (n = 36) had a restrictive left ventricular filling pattern (E deceleration time < 115 ms); group 2 (n = 43) had an E deceleration time > or = 115 ms. RESULTS: Patients in group 1 were significantly younger, in a higher New York Heart Association functional class, more frequently had a third heart sound and had a higher left ventricular filling pressure at catheterization. In addition, they showed more severe left and right ventricular dysfunction and dilation, a larger left atrium and more severe mitral regurgitation. A restrictive filling pattern was associated at Doppler study with a higher E wave velocity, lower A wave velocity and higher E/A ratio. During a follow-up interval of 22 +/- 14 months, all 14 patients who subsequently died or required heart transplantation showed a restrictive left ventricular filling pattern. At multivariate analysis, E deceleration time was the most powerful independent prognostic indicator of poor outcome or transplantation. CONCLUSIONS: Restrictive left ventricular filling pattern is frequent in dilated cardiomyopathy, is associated with more severe disease and is a powerful indicator of increased mortality risk and need for heart transplantation.

Persistence of restrictive left ventricular filling pattern in dilated cardiomyopathy: an ominous prognostic sign.

OBJECTIVES: We sought to assess the prognostic implications of the evolution of restrictive left ventricular filling pattern (RFP) in dilated cardiomyopathy (DCM). BACKGROUND: Previous work has demonstrated that a RFP in DCM is associated with a poor prognosis. Few data are available on the prognostic implications of the evolution of this pattern. METHODS: The evolution of left ventricular filling was studied by Doppler echocardiography in 110 patients with DCM. According to the left ventricular filling pattern at presentation and after 3 months of treatment, the patients were classified into three groups: Group 1A (n = 24) had persistent restrictive filling; Group 1B (n = 29) had reversible restrictive filling; and Group 2 (n = 57) had nonrestrictive filling. RESULTS: During follow-up (41 +/- 20 months), mortality plus heart transplantations was significantly higher in Group 1A than in Groups 1B and 2 (p < 0.0001). On multivariate analysis, the model incorporating E wave deceleration time at 3 months was more powerful at predicting mortality with respect to this variable at baseline (p = 0.0039). Clinical improvement at 1 and 2 years was significantly more frequent in Groups 1B and 2 than in Group 1A (p < 0.0001 at 2 years). CONCLUSIONS: In patients with DCM, the persistence of restrictive filling at 3 months is associated with a high mortality and transplantation rate. The patients with reversible restrictive filling have a high probability of improvement and excellent survival. Doppler echocardiographic reevaluation of these patients after 3 months of therapy gives additional prognostic information with respect to the initial study.

Long-term effects of carvedilol in idiopathic dilated cardiomyopathy with persistent left ventricular dysfunction despite chronic metoprolol. The Heart-Muscle Disease Study Group.

OBJECTIVES: The purpose of this study was to analyze whether long-term treatment with the nonselective beta-adrenergic blocking agent carvedilol may have beneficial effects in patients with dilated cardiomyopathy (DCM), who are poor responders in terms of left ventricular (LV) function and exercise tolerance to chronic treatment with the selective beta-blocker metoprolol. BACKGROUND: Although metoprolol has been proven to be beneficial in the majority of patients with heart failure, a subset of the remaining patients shows long-term survival without satisfactory clinical improvement. METHODS: Thirty consecutive DCM patients with persistent LV dysfunction (ejection fraction < or =40%) and reduced exercise tolerance (peak oxygen consumption <25 ml/kg/min) despite chronic (>1 year) tailored treatment with metoprolol and angiotensin-converting enzyme inhibitors were enrolled in a 12-month, open-label, parallel trial and were randomized either to continue on metoprolol (n = 16, mean dosage 142+/-44 mg/day) or to cross over to maximum tolerated dosage of carvedilol (n = 14, mean dosage 74+/-23 mg/day). RESULTS: At 12 months, patients on carvedilol, compared with those continuing on metoprolol, showed a decrease in LV dimensions (end-diastolic volume -8+/-7 vs. +7+/-6 ml/m2, p = 0.053; end-systolic volume -7+/-5 vs. +6+/-4 ml/m2, p = 0.047), an improvement in LV ejection fraction (+7+/-3% vs. -1+/-2%, p = 0.045), a reduction in ventricular ectopic beats (-12+/-9 vs. +62+/-50 n/h, p = 0.05) and couplets (-0.5+/-0.4 vs. +1.5+/-0.6 n/h, p = 0.048), no significant benefit on symptoms and quality of life and a negative effect on peak oxygen consumption (-0.6+/-0.6 vs. +1.3+/-0.5 ml/kg/min, p = 0.03). CONCLUSIONS: In DCM patients who were poor responders to chronic metoprolol, carvedilol treatment was associated with favorable effects on LV systolic function and remodeling as well as on ventricular arrhythmias, whereas it had a negative effect on peak oxygen consumption.

Quantitative texture analysis in two-dimensional echocardiography: application to the diagnosis of myocardial amyloidosis.

Qualitative and subjective analysis of two-dimensional echocardiographic images of the myocardial wall allows one to identify amyloid heart disease; the quantitative analysis of regional image texture might be an accurate method to differentiate normal from amyloid myocardial structures. To test this hypothesis, two-dimensional echocardiograms of nine normal subjects and six patients with histologically documented amyloid heart disease were evaluated. Quantitative texture measurements of the first order (mean gray level, skewness, kurtosis, energy and entropy) overlapped between the two groups. Among the second order statistics variables, entropy was significantly and consistently higher in amyloid versus normal patient data (septum in parasternal long-axis view: 6.3 +/- 0.3 versus 5.9 +/- 0.4; septum in apical four chamber view: 6.2 +/- 0.2 versus 5.8 +/- 0.3). Therefore, amyloid-involved myocardial walls show ultrasound image texture alterations that may be quantified with digital image analysis techniques.

Familial dilated cardiomyopathy: evidence for genetic and phenotypic heterogeneity. Heart Muscle Disease Study Group.

OBJECTIVES: This study was performed to evaluate the characteristics, mode of inheritance and etiology of familial dilated cardiomyopathy (FDC). BACKGROUND: A genetic form of disease transmission has been identified in a relevant proportion of patients with dilated cardiomyopathy (DCM). Variable clinical characteristics and patterns of inheritance, and an increased frequency of cardiac antibodies have been reported. An analysis of FDC may improve the understanding of the disease and the management of patients. METHODS: Of 350 consecutive patients with idiopathic DCM, 281 relatives from 60 families were examined. Family studies included clinical examination, electrocardiography, echocardiography and blood sampling. Of the 60 DCM index patients examined, 39 were attributable to FDC and 21 were due to sporadic DCM. Clinical features, histology, mode of inheritance and autoimmune serology were examined, molecular genetic studies were undertaken and the difference between familial and sporadic forms was analyzed. RESULTS: Only a younger age (p = 0.0005) and a higher ejection fraction (p = 0.03) could clinically distinguish FDC patients from those with sporadic DCM. However, a number of distinct subtypes of FDC were identified: 1) autosomal dominant, the most frequent form (56%); 2) autosomal recessive (16%), characterized by worse prognosis; 3) X-linked FDC (10%), with different mutations of the dystrophin gene; 4) a novel form of autosomal dominant DCM with subclinical skeletal muscle disease (7.7%); 5) FDC with conduction defects (2.6%), and 6) rare unclassifiable forms (7.7%). The forms with skeletal muscle involvement were characterized by a restrictive filling pattern; the forms with isolated cardiomyopathy had an increased frequency of organ-specific cardiac autoantibodies. Histologic signs of myocarditis were frequent and nonspecific. CONCLUSIONS: Familial dilated cardiomyopathy is frequent, cannot be predicted on a clinical or morphologic basis and requires family screening for identification. The phenotypic heterogeneity, different patterns of transmission, different frequencies of cardiac autoantibodies and the initial molecular genetic data indicate that multiple genes and pathogenetic mechanisms can lead to FDC.

Echocardiographic findings in myocarditis.

This study analyzes morphologic and functional alterations detected by M-mode and 2-dimensional echocardiography in 41 patients with histologically proven myocarditis and different clinical presentations: congestive heart failure (63%), atrioventricular block (17%), chest pain (15%) and supraventricular arrhythmias (5%). Left ventricular dysfunction was common (69%), particularly in patients with congestive heart failure (88%), often without or with minor cavity dilatation. Patients with atrioventricular block or chest pain had usually preserved ventricular function. Right ventricular dysfunction was present in 23%. Additional findings included asynergic ventricular areas (64%), left ventricular "hypertrophy" sometimes reversible (20%), hyperrefractile myocardial areas (23%), ventricular thrombi (15%) and "restrictive" ventricular filling (7%). It is concluded that echocardiographic features of myocarditis are polymorphous and nonspecific. The echocardiographic pattern can simulate alternatively dilated, hypertrophic, restrictive or "right" ventricular cardiomyopathy, as well as coronary artery disease. In an appropriate clinical context, echocardiography can be helpful in the diagnosis of myocarditis and in the selection of patients for endomyocardial biopsy.

Magnetic resonance imaging in right ventricular dysplasia.

Fifteen patients with right ventricular dysplasia were investigated by T1-weighted spin- and gradient-echo pulse sequences, using a protocol that enabled both a subjective analysis of myocardial signal intensity and a quantitative/qualitative analysis of right and left ventricular function. In 8 patients, 3 investigators independently recognized abnormally hyperintense areas in the anatomic sites usually affected by the disease. In 7 of these patients, these areas showed an overlap with a-dyskinetic areas imaged by both magnetic resonance imaging (MRI) and echocardiography. In 1 patient who underwent a cardiac transplant, MRI of the explanted heart showed an excellent correlation between the distribution of the lesions and the in vivo/in vitro features. The data were compared with those from an equivalent sample of patients affected by dilated cardiomyopathy. In the latter patients, no focal hyperintensities were attributed to any anatomic sites in the right ventricule, and no focal a-dyskinetic foci were observed. Furthermore, the 2 groups of patients were significantly different in regard to dimensional and functional quantitative parameters. The results suggest that MRI is useful in integrating echocardiographic data and can be helpful in diagnosing this disease in late stages.

Familial right ventricular dysplasia with biventricular involvement and inflammatory infiltration. Heart Muscle Disease Study Group.

The aetiology of right ventricular dysplasia/cardiomyopathy is presently unknown. A genetic background has been suggested, but myocarditis may play a part in its pathogenesis. Two familial cases of right ventricular dysplasia, one of whom had also a diagnosis of myocarditis, are reported. Both patients presented with ventricular arrhythmias. The father subsequently had a "flu-like" syndrome, heart failure, and biventricular dysfunction; "active" myocarditis was found at endomyocardial biopsy. Then the patient died suddenly. The daughter developed progressive biventricular dysfunction; then she was resuscitated from a cardiac arrest, and subsequently died suddenly. In both patients necropsy showed severe right ventricular atrophy and fibro-adipose substitution, associated with biventricular fibrosis. Inflammatory infiltration was also present in the first patient. This study shows the association of right ventricular dysplasia and myocarditis in the same family. These cases may represent a link between inherited and acquired ("inflammatory") forms of the disease.

Genetic factors in dilated cardiomyopathy.

Recent studies have demonstrated that genetic factors are likely to play a major role in the pathogenesis of idiopathic dilated cardiomyopathy (IDC). In clinical surveys, a familial trait has been demonstrated in 20 to 30% of idiopathic dilated cardiomyopathy patients (familial dilated cardiomyopathy). Molecular genetic studies have confirmed the clinical hypothesis of genetic heterogeneity in familial dilated cardiomyopathy, and are currently producing relevant advances in the understanding of this disease. The autosomal dominant form is considered to be the most frequent form of inherited idiopathic dilated cardiomyopathy. After the exclusion of a large series of candidate genes, the first familial dilated cardiomyopathy gene has been mapped to the long arm of chromosome 9. A second locus has been found on chromosome 1. Moreover, in two large families, characterized by a peculiar form of conduction delays and later development of myocardial dysfunction, the disease loci have been mapped to chromosome 1 and 3, respectively. The identification of the disease genes is in progress. In families with X-linked dilated cardiomyopathy, the disease gene has been identified as the dystrophin gene. The 5' end of the gene appears to be the critical region for the development of dilated cardiomyopathy without clinical evidence of muscle dystrophy. Furthermore, other cytoskeletal proteins, such as adhalin, could be involved in the pathogenesis of familial dilated cardiomyopathy. In familial right ventricular cardiomyopathy (or arrhythmogenic right ventricular dysplasia) characterized by isolated or prevalent right ventricular involvement, three different disease loci have been identified so far: two localized on the long arm of chromosome 14 and one on chromosome 1. The disease genes are still unknown and are currently under investigation. The study of the genetic factors at the molecular level is starting to elucidate the pathogenetic mechanisms of idiopathic dilated cardiomyopathy. These findings will also have relevant clinical and therapeutic implications.

Current perspective new insights into the molecular basis of familial dilated cardiomyopathy.

Genetic disease transmission has been identified in a significant proportion of patients with dilated cardiomyopathy (DCM). Variable clinical characteristics and patterns of inheritance, as well as recent molecular genetic data, indicate the existence of several genes causing the disease. Several distinct subtypes of familial DCM have been identified. Autosomal dominant DCM is the most frequent form (56% of our cases), and several candidate disease loci have been identified by linkage analysis. Three disease genes are presently known: the cardiac actin gene, the desmin gene, and the lamin A/C gene. This latter gene has recently been found to be responsible for both the autosomal dominant form of DCM with subclinical skeletal muscle disease (7.7% of cases) and the familial form with conduction defects (2.6% of cases) or the autosomal dominant variant of Emery-Dreifuss muscular dystrophy. The autosomal recessive form of DCM accounts for 16% of cases and is characterized by a worse prognosis. An X-linked form of DCM (10% of cases) manifests in the adult population and is due to mutations in the dystrophin gene. In the rare infantile form of DCM, mutations in the G4.5 gene have been identified. Finally, some of the rare unclassifiable forms (7.7% of cases) may be due to mitochondrial DNA mutations. Clinical and experimental evidence based on animal models suggest that, in a large number of cases, DCMs are diseases of the cytoskeleton. However, other causes, such as alterations in regulatory elements and in signaling molecules, are possible. Moreover, other genes called modifier genes can influence the severity, penetrance, and expression of the disease, and they will be a main objective of future investigations. Familial DCM is frequent, cannot be predicted on a clinical or morphological basis and requires family screening for identification. The advances in the genetics of familial DCM can allow improved diagnosis, prevention and genetic counseling, and represent the basis for the development of new therapies.

[New knowledge on the subject of therapy in cardiac decompensation in the light of large trials]. / Nuove conoscenze in tema di terapia dello scompenso cardiaco alla luce dei grandi trial.

Although an underlying disturbance in cardiac function can be identified in most patients with congestive heart failure, manifestations of the disease are greatly influenced by other factors, particularly neurohumoral and peripheral adaptive responses which occur secondary to impaired cardiac function. Until recently diuretic agents and digoxin formed the basis of conventional treatment of this condition. The majority of clinical trials published since 1980, indicate that digoxin lessens symptoms and reduces morbidity associated with congestive heart failure particularly in patients with more advanced symptoms and ventricular dysfunction. The efficacy of digitalis in congestive heart failure may in part result from sympathoinhibitory properties such as the activation of baroreceptorial mechanisms. At present there is no conclusive evidence that cardiac glycosides improve survival. Several trials clearly indicate that angiotensin converting enzyme inhibitors (enalapril, captopril) can reduce both morbidity and mortality in symptomatic congestive heart failure. Asymptomatic patients like those with severe left ventricular dysfunction and those who are at high risk for left ventricular remodeling after anterior wall myocardial infarction may also benefit from ACE-inhibition therapy. Increasing evidence suggests that beta-adrenergic blockade can produce symptomatic and hemodynamic improvement in heart failure of idiopathic and ischemic aetiology. Appropriately powered randomized controlled trials are required to determine the impact on survival of beta-blockers.

[Contribution of echocardiography to the diagnosis of patients with chronic heart failure]. / Contributo dell'ecocardiografia alla diagnosi eziologica nel paziente con scompenso cardiaco cronico.

The echocardiographic examination is generally performed in patients with heart failure and it often gives a significant contribution to the differential diagnosis. Firstly, the evaluation of left ventricular pump function by measuring the ejection fraction (EF) can distinguish patients with heart failure into two different groups, with depressed or preserved EF. The most frequent causes of heart failure and depressed EF are coronary artery disease, idiopathic dilated cardiomyopathy (DCM) and hypertensive heart disease. Although the echocardiographic features of coronary artery disease versus idiopathic DCM may be similar, the demonstration of inducible ischemia at dobutamine echocardiographic test suggests the presence of significant coronary artery disease and may be useful in the selection of cases for coronary arteriography. The association of left ventricular hypertrophy, hypokinesis and, sometimes, significant dilation is compatible with hypertensive heart disease or end-stage hypertrophic cardiomyopathy. No useful echocardiographic findings can identify the patients with genetic DCM or affected by myocarditis from other cases with idiopathic DCM. Some advanced cases of right ventricular dysplasia/cardiomyopathy may show a biventricular involvement and mimic DCM; these patients are usually characterized at echo by predominant right ventricular dilation and multiple a-dyskinetic bulges in the absence of pulmonary hypertension. Very difficult to manage are the patients with significant left ventricular dysfunction and severe valvular heart disease (such as aortic stenosis or mitral regurgitation). According to the literature, the left ventricular systolic function is relatively preserved (EF > 40%) in 30-40% of patients with heart failure. In these cases a diastolic dysfunction may be hypothesized. Echo-Doppler evaluation can be helpful in the recognition of signs of increased left ventricular stiffness ("restrictive filling pattern") and of increased filling pressures. In the differential diagnosis one must first consider the most frequent heart disorders that may present with this clinical syndrome, coronary artery disease and hypertensive heart disease. Furthermore, other less common diseases characterized by heart failure due to predominant diastolic dysfunction are the following: hypertrophic and restrictive cardiomyopathies, infiltrative heart diseases, such as amyloidosis, and constrictive pericarditis. Restrictive cardiomyopathy is characterized by heart failure and preserved left ventricular EF in the absence of significant ventricular dilation and hypertrophy; typical, although not pathognomonic, echocardiographic features are atrial enlargement ad restrictive filling pattern. In distinguishing constrictive pericarditis from restrictive cardiomyopathy useful Doppler signs are the wide respiratory variability in flow velocities at mitral and tricuspid levels, due to increased ventricular interdependence caused by the presence of an abnormally rigid pericardium.

[Heart failure due to diastolic dysfunction: the treatment principles]. / Scompenso cardiaco da disfunzione diastolica: principi di trattamento.

The clinical relevance of diastolic dysfunction in heart failure has recently been emphasized. In fact, the presence of signs of heart failure does not imply a depressed left ventricular systolic function; moreover, the severity of heart failure and effort tolerance are more closely related to diastolic than to systolic indexes. However, the principal trials about the treatment of heart failure were mainly addressed to patients with significant left ventricular systolic dysfunction, whereas the optimal therapy for diastolic dysfunction is not well known. The aim of this review was to assess the rationale and the therapeutic options in heart failure due to diastolic dysfunction. A diastolic dysfunction can be exclusive or associated with systolic dysfunction, as in dilated cardiomyopathy. It has to be noted that in this disease an improvement of diastolic function was demonstrated for most of the drugs currently employed in the treatment of heart failure, such as vasodilators, ACE inhibitors, beta-blockers, digitalis, and other inotropic drugs. Moreover, the favorable effect of the treatment on diastolic parameters (reduction of left ventricular filling pressure, regression of restrictive filling pattern) is associated with a positive prognostic impact. The main objective of the treatment of heart failure with preserved left ventricular systolic function is to control the symptoms by means of lowering high left ventricular filling pressure without significantly lowering cardiac output. According to the therapeutic guidelines of the American College of Cardiology/American Heart Association Task Force, the drugs indicated to treat symptomatic patients with heart failure and preserved left ventricular systolic function are diuretics and nitrates. Potentially useful, but with insufficiently proven efficacy are beta-blockers, calcium antagonists and ACE inhibitors, whereas direct vasodilators and inotropic drugs were considered inadvisable. It is important to remember that the treatment might possibly be oriented to the cause and also to the possible precipitating factors of the heart failure syndrome (i.e. ischemia, tachycardia, arrhythmias, hypertension). In conclusion, considering the relatively common incidence of heart failure due to prevalent diastolic dysfunction, and the few available data about the therapeutic options in these patients, large multicenter trials devoted to the treatment of this syndrome are needed.

[Echocardiographic follow-up of patients with heart failure. Which parameters should be measured? How often?]. / Il follow-up ecocardiografico del paziente con scompenso cardiaco. Quali parametri misurare? Con quale frequenza?

The echocardiographic evaluation keeps a relevant place in the evaluation of patients with heart failure and left ventricular systolic dysfunction, not only for its contribution to the diagnosis, prognostic stratification and comprehension of pathogenetic mechanisms, but also for the analysis of the evolution of the disease and the response to optimal medical therapy. On the other hand, the role of echocardiography in the follow-up of patients with diastolic dysfunction is still unclear. In patients with heart failure and left ventricular systolic dysfunction the analysis of changes in left ventricular function and dimension during follow-up is particularly relevant to recognize the potential benefit of optimal medical therapy with ACE-inhibitors and beta-blockers and their prognostic significance. The echo-Doppler hemodynamic evaluation is also of clinical and prognostic value particularly for the recognition of the persistence or (re)appearance of restrictive filling pattern during follow-up. Moreover, in patients with persistent severe left ventricular systolic dysfunction, the evaluation of right ventricular function may allow for the identification of a subset of patients at high risk for cardiovascular events. A practical flow-chart of echocardiographic assessment of patients with heart failure and left ventricular systolic dysfunction includes the following steps: 1) after 3 to 6 months on optimal therapy, to detect the persistence of restrictive filling pattern, if present at diagnosis; 2) after 12 to 24 months, to analyze the response of left ventricular function and dimension to optimal medical treatment; 3) serial examinations, according to the stage of the disease or to the episodes of worsening heart failure, to identify echocardiographic indicators of disease progression, such as worsening of left ventricular and/or right ventricular function or (re)appearance of restrictive filling pattern. The changes in these parameters seem to have a relevant prognostic significance to define the risk profile of patients with heart failure and left ventricular systolic dysfunction.

[Cardiac magnetic resonance. Optimization of the parameters in the evaluation of right and left ventricular function]. / La risonanza magnetica cardiaca. Ottimizzazione dei parametri nella valutazione della funzione ventricolare destra e sinistra.

MR imaging is the only non-invasive tomographic imaging modality capable of imaging the heart along planes that are parallel to each other and in any desired direction. Such reconstruction algorithms can thus be applied to MR images as the Simpson's rule which allows volume estimation of all cardiac cavities, although very irregular in shape, like the right ventricle. The authors optimized the technical parameters to obtain a set of multiphase double-angulated images on both the short and the long axes of the heart, in about 1-hour time. This technique was used to examine 31 patients suffering from several cardiopathies. The images allowed both end-diastolic and end-systolic volumes to be estimated, as well as the ejection fractions of both ventricles. In the left ventricle the area-length method and the Simpson's rule were applied, whereas only the latter was employed in the right ventricle. The correlation coefficients of US and MR data were, for the 3 parameters, r = 0.813, r = 0.920, and r = 0.879, respectively, in the first case, and r = 0.905, r = 0.923, and r = 0.890 in the second one. The time required to analyze the obtained data, which is done manually, is still considerably long.

Two-dimensional echocardiography during endomyocardial biopsy.

53 consecutive and unselected patients undergoing endomyocardial biopsy (EMB) had concomitant two-dimensional echocardiographic (2DE) and fluoroscopic control during 62 biopsy procedures (49 of the right, 13 of the left ventricle) in order to assess the capacity of 2DE to identify biopsy site, to allow a selective biopsy in different areas of the ventricles and to foresee a positive sampling. The echocardiographic documentation of a close contact of the bioptome tip with the ventricular wall was compared with the presence of endomyocardial tissue in the forceps of the bioptome. Contact of the bioptome tip with the endocardium was visualized in 86% of the right ventricular biopsies and in 85% of the left ventricular biopsies. Under 2DE monitoring it was possible to change the site of biopsy and selected areas were easily sampled. In a subgroup of 29 biopsies prospectively studied to assess the ability of 2DE to foresee positive sampling, the 2DE forecast was confirmed in 93% of the right and in 100% of the left ventricular samples. The apical view was more commonly used because it provides a good visualization of the bioptome tip and of intracardiac structures without interfering with concomitant fluoroscopic control. Our results suggest that 2DE monitoring during EMB may: 1) provide definite forceps position during the procedure in a large number of patients; 2) guide the bioptome to obtain samples from different and/or selected sites of the ventricles; 3) foresee a positive samples.