From Heart Failure to Highly Unsaturated Fatty Acid Deficiency and Vice Versa: Bidirectional Heart and Liver Interactions.

BACKGROUND: In several trials, beneficial prognostic effects of highly unsaturated fatty acids (HUFAs) in heart failure were shown. Because other studies showed no incremental benefit in nearly preserved cardiac function, the question arises, whether the degree of cardiac dysfunction is involved. It is hypothesized that increased left ventricular (LV) wall stress affects the endogenous hepatic HUFA metabolism, which in turn exhibits adverse cardiac consequences. METHODS: Cardiac magnetic resonance imaging was performed in 30 patients with suspected cardiomyopathy. The serum fatty acid profile was assessed using gas chromatography/mass spectrometry. RESULTS: Docosahexaenoic acid (DHA; P = 0.002) and eicosapentaenoic acid (EPA; by trend) levels were decreased in patients with reduced LV ejection fraction (≤ 50%) or LV dilatation (≥ 90 mL/m(2)). Decreased DHA (P = 0.003) and EPA (P = 0.022) levels were associated with a reduced LV ejection fraction. Decreased DHA level was correlated with increased end-diastolic (P = 0.047) and end-systolic LV wall stress (P = 0.001). Pseudocholinesterase activity was inversely correlated with end-diastolic (P = 0.020) and end-systolic LV wall stress (P = 0.025). CONCLUSIONS: DHA level was significantly reduced in heart failure. Similar, but less pronounced effects were found for EPA and arachidonic acid by trend. Increased LV wall stress was correlated with a reduced DHA level. Increased LV wall stress exhibits various adverse consequences (eg, increased oxygen consumption, favouring of arrhythmias, and an unfavourable remodelling). The increase of wall stress was paralleled by reduced HUFA level. Increased LV wall stress was correlated with reduced pseudocholinesterase, which is suggestive of hepatic congestion (ie, a cardiohepatic syndrome, involved in the altered fatty acid profile in heart failure) and has major consequences regarding the dose-efficacy of HUFA treatment.

Wall stress determines systolic and diastolic function--Characteristics of heart failure.

INTRODUCTION: Heart failure can be caused by systolic or diastolic dysfunction. Diagnosing diastolic dysfunction remains challenging, although several criteria have been identified. Ventricular wall stress is crucially involved. It is hypothesized whether increased end-diastolic and end-systolic ventricular wall stress as assessed by the wall stress index is associated with cardiac dysfunction and thus provide novel diagnostic criteria. METHODS: 1050 consecutive patients with suspected non-ischemic heart failure covering a broad spectrum from normal to severely impaired cardiac function were observed. Cardiac magnetic resonance imaging was performed to assess left ventricular (LV) volumes, myocardial mass, peak ejection (PER) and filling rate (PFR). RESULTS: A reduced PFR was found in 348 patients (33.1%), which resulted from 275 of 422 patients (65.2%) with reduced and from 73 of 628 patients (11.6%) with preserved LVEF (p<0.0001). Increased LV volume and mass was correlated with reduced PER and PFR (p<0.0001). Increased end-diastolic wall stress was the strongest predictor of a reduced PER (OR 4.5 [2.6 to 7.8], p<0.0001) and increased end-systolic wall stress predicted a reduced PFR (OR 1.2 [1.1 to 1.3], p<0.0001). Increased end-systolic wall stress was correlated with increased pulmonary pressure (p<0.0001). Normal end-systolic wall stress<18 kPa had a favorable predictive value for the absence of an impaired filling and increased pulmonary capillary pressure. CONCLUSION: Increased end-diastolic wall stress precedes a reduced ventricular ejection rate and increased end-systolic wall stress determines an impaired diastolic filling. It is thus suggested to add assessment of ventricular wall stress as diagnostic criterion of heart failure.

Airflow limitation in COPD is associated with increased left ventricular wall stress in coincident heart failure.

BACKGROUND: COPD and heart failure occur with a considerable coincidence. Beside well-known mechanisms of increased right heart load in COPD, dedicated changes of the left ventricle (LV) are ill-defined and the question remains, whether specific interactions exist beyond common shared risk factors. METHODS: LV wall stress was calculated based on cardiac magnetic resonance imaging in 28 patients with COPD (GOLD I to III) and coexistent heart failure (LVEF 42 ± 19%) due to non-ischaemic and ischaemic cardiomyopathy. RESULTS: LV enddiastolic (p = 0.048) and endsystolic wall stress (p = 0.034) increased from GOLD stage I to III. Reduced FEV1 was correlated with increased enddiastolic (p = 0.0210) and endsystolic LV volume (p = 0.0413) and with increased enddiastolic (p = 0.0161) and endsystolic LV wall stress (p = 0.0315), respectively. Increased wall stress was associated with a decreased FEV1/FVC ratio. CONCLUSIONS: The severity of airflow limitation in COPD was correlated with increased LV wall stress. It is suggested that respiration in pulmonary obstruction is associated with an increased negative intrathoracic pressure when compared with normal lung function, which is transmitted to the heart and increases the transmural pressure gradient and thereby distending forces on the heart. Increased ventricular wall stress is known to be associated with a broad variety of unfavourable consequences, which should be taken into account to contribute to a worse prognosis in COPD.

Occurrence and positive predictive value of additional nonmass findings for risk stratification of breast microcalcifications in mammography.

PURPOSE: To assess the occurrence and positive predictive value of additional nonmass findings to stratify the risk of breast microcalcifications. METHODS: This retrospective evaluation included 278 lesions with vacuum- or image-guided hook-wire biopsy for suspicious microcalcifications. The lesions were categorized into exclusive microcalcifications and microcalcifications with focal asymmetry, tubular density or architectural distortion (ie, nonmass findings). To evaluate the utility of additional nonmass findings for risk stratification, outcome variables were positive predictive values and odds ratios for malignancy and invasive carcinoma. RESULTS: Forty-five of 278 microcalcification lesions (16%) were associated with nonmass findings: 28 focal asymmetries, 2 tubular densities, and 15 focal asymmetries in conjunction with tubular densities. Architectural distortion was observed in 28 of these cases. The odds ratio for additional nonmass findings relative to exclusive microcalcifications was 5.9 and was statistically significant (P < .00001). Architectural distortion was the most specific indicator for malignancy and invasiveness, with odds ratios of 6.5 (P = .0072) and 5.6 (P = .0214), respectively. CONCLUSIONS: Microcalcifications with nonmass findings were less frequent than exclusive microcalcifications but were more predictive for malignancy. Architectural distortion demonstrated the highest risk of malignancy and invasiveness. Assessment of additional nonmass findings might be useful for further risk stratification of microcalcifications, indications for additional imaging, and pretreatment considerations.

MR, CT, and PET imaging in pericardial disease.

Although echocardiography remains the standard diagnostic tool for identifying pericardial diseases, procedures with better delineation of morphology and heart function are often required. The pericardium consists of an inner visceral (epicardium) and outer parietal layer (pericardium), which constitute for the pericardial cavity. Pericardial effusion can occur as transudate, exudate, pyopneumopericardium, or hemopericardium. Potential causes are inflammatory processes, that is, pericarditis due to autoimmune or infective reasons, neoplasms, irradiation, or systemic disorders, chronic renal failure, endocrine, or metabolic diseases. Pericardial fat can mimic pericardial effusion. Using various image-acquisition sequences, MRI allows identifying and separating fluid and solid structures. Fast spin-echo T1-weighted sequences with black-blood preparation are favourably used for morphological evaluation. Fast spin-echo T2-weighted sequences, particularly with fat saturation, and short-tau inversion-recovery sequences are useful to visualize oedema and inflammation. For further tissue characterization, delayed inversion-recovery imaging is used. Therefore, image acquisition is performed at 5-20 min subsequent to contrast agent administration, the so-called technique of late gadolinium enhancement. Ventricular volumes and myocardial mass can be assessed accurately by steady-state free-precession sequences, which is required to measure cardiac function and ventricular wall stress. Constrictive pericarditis usually results from chronic inflammatory processes leading to increased stiffness, which impedes the slippage of both pericardial layers and thereby the normal cardiac filling. CT imaging can favourably assess pericardial calcification. Thus, MR and CT imaging allow a comprehensive delineation of the pericardium. Superior to echocardiography, both methods provide a larger field of view and depiction of the complete chest including abnormalities of the surrounding mediastinum and lungs. PET provides unique information on the in vivo metabolism of 18-fluorodeoxyglucose that can be superimposed on CT findings and is useful for identifying inflammatory processes or masses, for example neoplasms. These imaging techniques provide advanced information of anatomy and cardiac function to optimize the pericardial access, for example by the AttachLifter system, for diagnosis and treatment.

Increased end diastolic wall stress precedes left ventricular hypertrophy in dilative heart failure--use of the volume-based wall stress index.

INTRODUCTION: To examine a potential interrelation of left ventricular (LV) wall stress and hypertrophy, we assessed increased wall stress in patients with suspected non-ischemic dilative cardiomyopathy and addressed the question whether increased LV wall stress is involved in the development of LV hypertrophy. METHODS: We studied 502 consecutive patients in whom LV mass, LV enddiastolic (LVEDV) and endsystolic volume (LVESV) was determined using cardiac magnetic resonance (CMR). Based on a thick-walled sphere, we introduced a myocardial and cavity volume-based wall stress index. Follow up CMR examinations were obtained in a representative subgroup of 71 patients. RESULTS: LV mass was correlated with LVEDV (r=0.517, P<0.001) and LVESV (r=0.510, P<0.001). Despite LV hypertrophy, LV mass was not sufficient to compensate for LV dilatation resulting in an increased wall stress. Increased LV enddiastolic wall stress was found in 227 patients (45 %) and increased endsystolic wall stress in 198 (39 %). In patients with normal LV enddiastolic wall stress ≤ 4 kPa at time of enrolment, no changes of LV mass occurred during follow up (142 ± 46 g vs. 141 ± 47 g). In contrast, patients with initially increased LV enddiastolic wall stress >4 kPa developed greater LV hypertrophy (141 ± 48 g vs. 158 ± 60 g, P=0.0247). CONCLUSIONS: LV wall stress can be derived from CMR measurements of LV myocardium and cavity using the volume-based wall stress index. Increased LV enddiastolic wall stress leads to LV hypertrophy. Beyond a certain degree of LV dilatation, the extent of hypertrophy does not compensate LV dilatation. The ensuing increased wall stress promotes dilatation and consecutively hypertrophy with an unfavorable prognosis. It is proposed to use the volume-based wall stress index as new diagnostic criterion in heart failure.

Occurrence of late gadolinium enhancement is associated with increased left ventricular wall stress and mass in patients with non-ischaemic dilated cardiomyopathy.

AIMS: Occurrence of late gadolinium enhancement (LGE) as assessed by cardiac magnetic resonance (CMR) imaging has been attributed to various myocardial injuries. We hypothesized that LGE is associated with left ventricular (LV) wall stress. METHODS AND RESULTS: We examined 300 patients with suspected non-ischaemic dilated cardiomyopathy. Cardiac magnetic resonance was used to assess LV volume, mass, wall stress, and LGE. Increased LV end-diastolic wall stress (> 4 kPa) was found in 112 patients (37 %), and increased end-systolic wall stress (>18 kPa) in 121 patients (40%). Presence of LGE was observed in 93 patients (31%). End-diastolic (94 ± 43 vs. 79 ± 42 ml/m(2), P = 0.006) and end-systolic LV volumes (62 ± 44 vs. 44 ± 37 ml/m(2), P < 0.001) and LV mass (95 ± 34 vs. 78 ± 31 g/m(2), P < 0.001) were increased in patients exhibiting LGE. In particular, LV end-diastolic and end-systolic wall stress were increased (4.5 ± 2.8 vs. 3.6 ± 3.0 kPa, P = 0.025; 19.6 ± 9.1 vs. 17.5 ± 8.2 kPa, P = 0.045). Late gadolinium enhancement was observed more frequently than would be expected from random occurrence in patients with increased end-diastolic (39 vs. 26%, P = 0.020) and end-systolic wall stress (41 vs. 24%, P = 0.002). Both normal end-diastolic and end-systolic wall stress had a high negative predictive value for LGE (75 and 76%). CONCLUSIONS: The present study shows that occurrence of LGE in cardiomyopathy is associated with increased LV wall stress and mass. Suspected causes are an increased capillary leakage by stretch, impaired contrast agent redistribution, or increased diffusion distances. It is proposed that LGE should be considered as a potential prognostic determinant of heart failure and severe arrhythmias.

Prospective comparison of image quality and diagnostic accuracy of 0.5 molar gadobenate dimeglumine and 1.0 molar gadobutrol in contrast-enhanced run-off magnetic resonance angiography of the lower extremities.

PURPOSE: To compare image quality and diagnostic accuracy of 0.5 molar gadobenate dimeglumine and 1.0 molar gadobutrol in contrast-enhanced (CE) magnetic resonance angiography (MRA) of the lower extremities interindividually. MATERIALS AND METHODS: The study was approved by our Institutional Review Board. Written informed consent was obtained from all patients before enrollment in the study. We prospectively included 74 patients (21 women, 53 men; mean age ± SD: 67.9 ± 11.0 years) with suspected peripheral occlusive vascular disease. All patients underwent a contrast-enhanced MRA of both lower extremities with either 0.1 mL/kg body weight gadobutrol or gadobenate dimeglumine. Image quality, stenosis grade, and artifacts were assessed by two blinded, independent investigators. Signal intensity (SI), signal-to-noise ratio (SNR), and contrast-to-noise ratio (CNR) were measured by a third investigator. Contrast agent groups were compared to each other using a two-sided Student's t-test. RESULTS: The results did not show significant differences for SI, SNR, or CNR. Both investigators were in significant accordance (P < 0.05) with regard to stenosis detection. CONCLUSION: We conclude that application of standard clinical doses (0.1 mL/kg body weight) of both contrast agents provides similar diagnostic results and gadolinium dose could be reduced by the application of a single dose of gadobenate dimeglumine for CE run-off MRA.

Association of hyperhomocysteinemia with left ventricular dilatation and mass in human heart.

BACKGROUND: Hyperhomocysteinemia is a risk factor for ischemic heart disease. Several other mechanisms apply also to dilative types of heart failure of various, non-ischemic etiologies. We hypothesized that hyperhomocysteinemia is associated with left ventricular (LV) dilatation and hypertrophy in dilative cardiomyopathy. METHODS: Homocysteine was measured in 66 individuals with suspected cardiomyopathy. Cardiac magnetic resonance imaging was used to assess LV volume, mass, and wall stress. RESULTS: Hyperhomocysteinemia (> 12 micromol/L) was found in 45 patients (68%). LV mass was greater in these patients compared with individuals with normal homocysteine (83+/-27 vs. 67+/-19 g/m(2); p<0.02). Homocysteine was increased in patients with increased brain natriuretic peptide > or = 100 pg/mL (18.3+/-5.9 vs. 14.9+/-5.1 micromol/L; p=0.018). LV mass, LV end-diastolic and end-systolic volume (LVEDV, LVESV) were significantly increased in individuals in the upper quartile compared with the lower quartile (90+/-25 vs. 65+/-18 g/m(2), p=0.021; 114+/-50 vs. 71+/-23 mL/m(2), p=0.042; 76+/-51 vs. 36+/-22 mL/m(2), p=0.045). LV dilatation (LVEDV > or = 90 mL/m(2)) was more common in hyperhomocysteinemia (> 12 micromol/L, p=0.0166). Normalized LV mass was correlated with homocysteine (r=0.346, p=0.065). Homocysteine was not significantly correlated with LVEDV (r=0.229, p=0.065), LV end-diastolic wall stress (r=0.226, p=0.069) and LV ejection fraction. CONCLUSIONS: Hyperhomocysteinemia appears to be, at least in part, involved in a disproportional LV dilatation, where the ensuing hypertrophy is not sufficient to compensate for the increased wall stress. A potential mechanism is the hyperhomocysteinemia associated increase in oxidative stress that favors muscle fiber slippage.

Accuracy of MRI volume measurements of breast lesions: comparison between automated, semiautomated and manual assessment.

The aim of this study was to investigate the efficacy of a dedicated software tool for automated and semiautomated volume measurement in contrast-enhanced (CE) magnetic resonance mammography (MRM). Ninety-six breast lesions with histopathological workup (27 benign, 69 malignant) were re-evaluated by different volume measurement techniques. Volumes of all lesions were extracted automatically (AVM) and semiautomatically (SAVM) from CE 3D MRM and compared with manual 3D contour segmentation (manual volume measurement, MVM, reference measurement technique) and volume estimates based on maximum diameter measurement (MDM). Compared with MVM as reference method MDM, AVM and SAVM underestimated lesion volumes by 63.8%, 30.9% and 21.5%, respectively, with significantly different accuracy for benign (102.4%, 18.4% and 11.4%) and malignant (54.9%, 33.0% and 23.1%) lesions (p < 0.05). Inter- and intraobserver reproducibility was best for AVM (mean difference +/- 2SD, 1.0 +/- 9.7% and 1.8 +/- 12.1%) followed by SAVM (4.3 +/- 25.7% and 4.3 +/- 7.9%), MVM (2.3 +/- 38.2% and 8.6 +/- 31.8%) and MDM (33.9 +/- 128.4% and 9.3 +/- 55.9%). SAVM is more accurate for volume assessment of breast lesions than MDM and AVM. Volume measurement is less accurate for malignant than benign lesions.