Delayed enhancement imaging in a contemporary patient cohort following correction of tetralogy of Fallot

2014 ◽  
Vol 25 (7) ◽  
pp. 1268-1275 ◽  
Author(s):  
Uta Preim ◽  
Philipp Sommer ◽  
Janine Hoffmann ◽  
Jana Kehrmann ◽  
Lukas Lehmkuhl ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Tetralogy Of Fallot ◽  
Nyha Class ◽  
Left Ventricular ◽  
Delayed Enhancement ◽  
Volume Index ◽  
Delayed Enhancement Imaging ◽  
The Right ◽  
Myocardial Scars

AbstractObjectiveTo test the hypothesis that myocardial scars after repair of tetralogy of Fallot are related to impaired cardiac function and adverse clinical outcome.MethodsA total of 53 patients were retrospectively analysed after repair of tetralogy of Fallot. The median patient age was 20 years (range 2–48).Cardiac MRI with a 1.5 T magnet included cine sequences to obtain volumes and function, phase-sensitive inversion recovery delayed enhancement imaging to detect myocardial scars, and flow measurements to determine pulmonary regurgitation fraction. In addition, clinical parameters were obtained.ResultsAn overall 83% of patients were in NYHA class I. All patients with the exception of 2 (96%) had pulmonary insufficiency. Mean ejection fraction and end-diastolic volume index were 46% and 128 ml/m2 for the right ventricle and 54% and 82 ml/m2 for the left ventricle, respectively. Excluding enhancement of the septal insertion and prosthetic patches, delayed enhancement was seen in 11/53 cases (21%). Delayed enhancement of the right ventricle was detected in 6/53 patients (11%) and of the left ventricle in 5/53 patients (9%). The patient group with delayed enhancement was significantly older (p=0.003), had later repair (p=0.007), and higher left ventricular myocardial mass index (p=0.009) compared with the group without delayed enhancement.ConclusionsThis study reveals that scarring is common in patients after surgical repair of tetralogy of Fallot and is associated with older age and late repair. However, there was no difference in right ventricular function, NYHA class, or occurrence of clinically relevant arrhythmias between patients with and those without myocardial scars.

Regulation of K+ and Ca2+ channels in experimental cardiac failure

1991 ◽  
Vol 261 (6) ◽  
pp. H1979-H1987 ◽  
Author(s):  
M. Gopalakrishnan ◽  
D. J. Triggle ◽  
A. Rutledge ◽  
Y. W. Kwon ◽  
J. A. Bauer ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Cardiac Failure ◽  
Radioligand Binding ◽  
Weight Ratio ◽  
Left Ventricular ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
The Right

To examine the status of ATP-sensitive K+ (K+ATP) channels and 1,4-dihydropyridine-sensitive Ca2+ (Ca2+DHP) channels during experimental cardiac failure, we have measured the radioligand binding properties of [3H]glyburide and [3H]PN 200 110, respectively, in tissue homogenates from the rat cardiac left ventricle, right ventricle, and brain 4 wk after myocardial infarction induced by left coronary artery ligation. The maximal values (Bmax) for [3H]glyburide and [3H]PN 200 110 binding were reduced by 39 and 40%, respectively, in the left ventricle, and these reductions showed a good correlation with the right ventricle-to-body weight ratio in heart-failure rats. The ligand binding affinities were not altered. In the hypertrophied right ventricle, Bmax values for both the ligands were not significantly different when data were normalized to DNA content or right ventricle weights but showed an apparent reduction when normalized to unit protein or tissue weight. Moderate reductions in channel densities were observed also in whole brain homogenates from heart failure rats. Assessment of muscarinic receptors, beta-adrenoceptors and alpha 1-adrenoceptors by [3H]quinuclidinyl benzilate, [3H]dihydroalprenolol, and [3H]prazosin showed reductions in left ventricular muscarinic and beta-adrenoceptor densities but not in alpha 1-adrenoceptor densities, consistent with earlier observations. It is suggested that these changes may in part contribute to the pathology of cardiac failure.

Ventricular systolic interdependence: volume elastance model in isolated canine hearts

1987 ◽  
Vol 253 (6) ◽  
pp. H1381-H1390 ◽  
Author(s):  
W. L. Maughan ◽  
K. Sunagawa ◽  
K. Sagawa
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Cross Talk ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Ventricular Free Wall ◽  
Free Wall ◽  
Right Ventricular Free Wall ◽  
Systolic Volume ◽  
The Right

To analyze the interaction between the right and left ventricle, we developed a model that consists of three functional elastic compartments (left ventricular free wall, septal, and right ventricular free wall compartments). Using 10 isolated blood-perfused canine hearts, we determined the end-systolic volume elastance of each of these three compartments. The functional septum was by far stiffer for either direction [47.2 +/- 7.2 (SE) mmHg/ml when pushed from left ventricle and 44.6 +/- 6.8 when pushed from right ventricle] than ventricular free walls [6.8 +/- 0.9 mmHg/ml for left ventricle and 2.9 +/- 0.2 for right ventricle]. The model prediction that right-to-left ventricular interaction (GRL) would be about twice as large as left-to-right interaction (GLR) was tested by direct measurement of changes in isovolumic peak pressure in one ventricle while the systolic pressure of the contralateral ventricle was varied. GRL thus measured was about twice GLR (0.146 +/- 0.003 vs. 0.08 +/- 0.001). In a separate protocol the end-systolic pressure-volume relationship (ESPVR) of each ventricle was measured while the contralateral ventricle was alternatively empty and while systolic pressure was maintained at a fixed value. The cross-talk gain was derived by dividing the amount of upward shift of the ESPVR by the systolic pressure difference in the other ventricle. Again GRL measured about twice GLR (0.126 +/- 0.002 vs. 0.065 +/- 0.008). There was no statistical difference between the gains determined by each of the three methods (predicted from the compartment elastances, measured directly, or calculated from shifts in the ESPVR). We conclude that systolic cross-talk gain was twice as large from right to left as from left to right and that the three-compartment volume elastance model is a powerful concept in interpreting ventricular cross talk.

P5272Right versus Left Ventricular Remodelling after Surgical myectomy for HOCM

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Abdelkhalek ◽  
A El Sawy ◽  
R Doss ◽  
A Samaan ◽  
M Donia ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Nyha Class ◽  
Left Ventricular ◽  
P Value ◽  
Peak Strain ◽  
Functional Changes ◽  
Septal Myectomy ◽  
Surgical Myectomy ◽  
The Right

Abstract Background Surgical myectomy for (HOCM) results in complex structural and functional changes. “Remodelling” in different cardiac chambers. To date, changes in the Right versus the left Ventricle have not been studied. Methods Fourty five patients (mean age = 32±16, 68% males) who underwent extended septal myectomy for LVOTO and Fourty “normal” controls (mean age = 32±12 years, 52% males) were studied by cardiac magnetic resonance imaging (CMR). The patients were studied pre-operatively and 6–18 months post-operatively (median = 9 months). The images were analysed by both commercial and in-house software. Results After myectomy. Follow up CMR showed changes in RV mass (21±5 to 23±7) g/m2, volume (60±15 to 66±12) ml/m2 and shape using 3 different methods. RV deformation parameters showed significant changes with circumferential strain (−8±2 to −14±4), filling (38±16 to 62±19) ml/s/m2 and ejection rate (−44±17 to −75±22). Changes in RV were substantially higher than those observed in the LV (Figure. 1, Table. 1). All patients reported significant symptomatic improvement with 31 (78%) patients in NYHA class I and 9 (22%) in class II at follow up. Significant reduction in peak gradient across the LVOT by 75%. Table 1. Summary of reported parameters related to RV Shape for pre and post operation HOCM patients and Normal Healthy Volunteers LV RV Pre Post Normal P-value Pre Post Normal P-value EDV ml/m2 75±18 81±14 73±10 0.005 60±15 66±12 71±12 0.002 ESV ml/m2 20±9 24±8 26±6 0.008 16±7 19±9 26±7 0.02 SV ml/m2 56±13 57±10 51±13 0.38 44±11 48±10 49±14 0.009 EF 74±7 70±7 65±5 0.001 74±8 72±7 64±6 0.228 Mass g/m2 74±33 62±29 27±8 0.0456 21±5 23±7 18±5 0.2100 PFR ml/m2 173±48 141±48 141±40 <0.0001 38±16 62±19 55±24 <0.0001 PER ml/m2 −179±35 −172±42 −144±42 0.29 −44±17 −75±22 −57±22 <0.0001 Peak Strain −20±3 −20±3 −20±3 0.49 −8±2 −14±4 −12±3 <0.0001 Conclusion LV septal myectomy is followed by structural and functional remodelling which is more extensive in the right than the left ventricle. The clinical significance of these findings needs further study.

scholarly journals Genomic modulation of mitochondrial respiratory genes in the hypertrophied heart reflects adaptive changes in mitochondrial and contractile function

2007 ◽  
Vol 293 (5) ◽  
pp. H2819-H2825 ◽  
Author(s):  
Makhosazane Zungu ◽  
Maria Pilar Alcolea ◽  
Francisco José García-Palmer ◽  
Martin E. Young ◽  
M. Faadiel Essop
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Respiratory Function ◽  
Hypobaric Hypoxia ◽  
Contractile Function ◽  
Left Ventricular ◽  
Transcript Levels ◽  
Mitochondrial Number ◽  
The Right ◽  
Mitochondrial Respiratory

We hypothesized the coordinate induction of mitochondrial regulatory genes in the hypertrophied right ventricle to sustain mitochondrial respiratory capacity and contractile function in response to increased load. Wistar rats were exposed to hypobaric hypoxia (11% O2) or normoxia for 2 wk. Cardiac contractile and mitochondrial respiratory function were separately assessed for the right and left ventricles. Transcript levels of several mitochondrial regulators were measured. A robust hypertrophic response was observed in the right (but not left) ventricle in response to hypobaric hypoxia. Mitochondrial O2 consumption was increased in the right ventricle, while proton leak was reduced vs. normoxic controls. Citrate synthase activity and mitochondrial DNA content were significantly increased in the hypertrophied right ventricle, suggesting higher mitochondrial number. Transcript levels of nuclear respiratory factor-1, peroxisome proliferator-activated receptor-γ-coactivator-1α, cytochrome oxidase (COX) subunit II, and uncoupling protein-2 (UCP2) were coordinately induced in the hypertrophied right ventricle following hypoxia. UCP3 transcript levels were significantly reduced in the hypertrophied right ventricle vs. normoxic controls. Exposure to chronic hypobaric hypoxia had no significant effects on left ventricular mitochondrial respiration or contractile function. However, COXIV and UCP2 gene expression were increased in the left ventricle in response to chronic hypobaric hypoxia. In summary, we found coordinate induction of several genes regulating mitochondrial function and higher mitochondrial number in a model of physiological right ventricular hypertrophy, linking the efficiency of mitochondrial oxidative phosphorylation and respiratory function to sustained contractile function in response to the increased load.

scholarly journals Epigenetics, inflammation and metabolism in right heart failure associated with pulmonary hypertension

2017 ◽  
Vol 7 (3) ◽  
pp. 572-587 ◽  
Author(s):  
Nolwenn Samson ◽  
Roxane Paulin
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Pressure Overload ◽  
Right Heart Failure ◽  
Left Ventricular ◽  
Ventricular Failure ◽  
Pulmonary Arterial ◽  
Ventricle Hypertrophy ◽  
The Right

Right ventricular failure (RVF) is the most important prognostic factor for both morbidity and mortality in pulmonary arterial hypertension (PAH), but also occurs in numerous other common diseases and conditions, including left ventricle dysfunction. RVF remains understudied compared with left ventricular failure (LVF). However, right and left ventricles have many differences at the morphological level or the embryologic origin, and respond differently to pressure overload. Therefore, knowledge from the left ventricle cannot be extrapolated to the right ventricle. Few studies have focused on the right ventricle and have permitted to increase our knowledge on the right ventricular-specific mechanisms driving decompensation. Here we review basic principles such as mechanisms accounting for right ventricle hypertrophy, dysfunction, and transition toward failure, with a focus on epigenetics, inflammatory, and metabolic processes.

Alterations in ventricular excitability in conscious dogs during development of chronic heart failure

1986 ◽  
Vol 250 (6) ◽  
pp. H1022-H1029 ◽  
Author(s):  
C. W. White ◽  
M. J. Mirro ◽  
D. D. Lund ◽  
D. J. Skorton ◽  
N. G. Pandian ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Time Course ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Maximum Increase ◽  
Electrophysiological Properties ◽  
Cycle Lengths ◽  
The Right

Arrhythmias in patients with heart failure may result from altered electrophysiological properties of the myocardium. To examine changes in ventricular excitability during cardiac failure and to relate these changes to ventricular structural and neurochemical abnormalities, right ventricular failure was produced in dogs by pulmonary artery banding and by creating tricuspid regurgitation. Right and left ventricular excitability thresholds were tested biweekly in heart failure (HF) and sham-operated conscious dogs by means of strength-duration curves (1-40 ms) at basic cycle lengths (BCL) of 300-500 ms until time of death (21-188 days). Marked increases in the excitability threshold of the right ventricle occurred in HF (mean maximum % increase, 205 +/- 42 at BCL 500 ms). Smaller, though significant increases in the left ventricular excitability threshold in HF were also seen (mean maximum % increase 103 +/- 36 at BCL 500 ms). Increases in the excitability threshold of the left as well as the right ventricles occurred, even though ventricular dilation (2-D Echo) was confined to the right ventricle. The time course of changes in the excitability threshold was variable (maximum occurrence at 21 +/- 3 days right ventricle, 23 +/- 11 days left ventricle). Tyrosine hydroxylase activity and norepinephrine content of the right ventricle were markedly depleted at death, when the excitability threshold was high. Similar though nonsignificant trends in reductions of these sympathetic neurochemicals were seen in the left ventricle. Levels of choline acetyltransferase and QNB binding in both ventricles were unaffected.

Growth of the Heart and Lungs in Hypoxic Rodents: A Model of Human Hypoxic Disease

1974 ◽  
Vol 46 (3) ◽  
pp. 375-391 ◽  
Author(s):  
Carolin Hunter ◽  
Gwenda R. Barer ◽  
J. W. Shaw ◽  
E. J. Clegg
Keyword(s):  
Body Weight ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Left Ventricular ◽  
Muscle Fibre Size ◽  
Littermate Control ◽  
Normal Environment ◽  
The Right ◽  
Rats And Mice ◽  
The Relationship

1. Rats and mice were kept in a decompression chamber at 52 kPa (390 mmHg) for 1–4 weeks and their hearts and lungs were compared with littermate control animals. In both species growth was retarded in the hypoxic environment. 2. In both species small peripheral lung vessels became thickened, developing two elastic laminae with a muscular coat between. A method was developed for assessing these changes in large numbers of animals. The number of thick-walled vessels was still high after 4 weeks' recovery in a normal environment. Pulmonary vascular resistance, measured by a perfusion method, increased in animals kept in the decompression chamber. 3. Mouse lungs became heavier than controls; the increase was not due to a greater fluid content. Rat lungs were heavy in relation to body weight but not heavier than controls; there may have been slight thickening of alveolar walls. Chest areas, measured from radiographs, were large relative to body weight in hypoxic rats. 4. The relationship between right and left ventricular weight and body weight was studied in normal rats and mice. The left ventricle grew about four times more quickly than the right. Changes in ventricular weights during exposure in the decompression chamber and subsequent recovery in a normal environment were related to these normal growth curves. 5. In both species the right ventricle grew abnormally fast in the decompression chamber. It was absolutely heavier than that of controls and relative to body weight was extremely heavy. After 4 weeks' recovery the relationship between right ventricular weight and body weight was nearly normal; this was achieved by retarded growth or actual loss of weight. 6. In mice the left ventricle grew normally in the decompression chamber and was heavy in relation to body weight. In rats its growth was retarded in the chamber and was normal in relation to body weight. 7. Morphometry of the hypertrophied right ventricle showed that muscle fibre size and total muscle mass had increased in hypoxic rats. There had been no increase in nuclear mass, but the perinuclear sarcoplasm had increased. All layers of the myocardium participated in the hypertrophy.

scholarly journals Myocardial tissue function and characterization in patients with idiopathic cardiac magnetic resonance myopericarditis: evolutionary analysis

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
A Soeiro ◽  
A S Bossa ◽  
M C Cesar ◽  
T C A T Leal ◽  
G Garcia ◽  
...  
Keyword(s):  
Right Ventricle ◽  
Tissue Characterization ◽  
Late Enhancement ◽  
Left Ventricular ◽  
Volume Index ◽  
Systolic Volume ◽  
End Systolic Volume ◽  
The Right

Abstract Introduction The identification of prognostic markers related to the occurrence of events and recovery of ventricular function may be important in patients with acute myopericarditis (AMP). There is still a lack of data related to tissue characterization by cardiac magnetic resonance (CMR) of AMP, evolution and definition of possible long-term prognostic markers. Purpose To evaluate the myocardial tissue characterization of CMR related to the occurrence of combined events (death from all causes, heart failure and AMP recurrence) and the increase in left ventricular ejection fraction (LVEF) in patients with AMP. Methods Inclusion criteria were chest pain and/or electrocardiographic changes associated with elevated troponin (above the 99th percentile) in the absence of coronary stenosis and diagnosis of AMP by CMR &lt;48 hours of admission confirmed by the presence of edema and/or late enhancement. After a follow-up of up to 24 months, 100 patients remained and in the assessment of the increase in LVEF (increase &gt;5%), 36 cases remained, recalled for a new CMR between 6 and 18 months from the initial event. Results Significant differences in CMR were found between patients who had combined events (n=26) versus no combined events (n=74) in the following characteristics evaluated: initial LVEF (OR=0.938; CI: 0.895–0.984, p=0.008), left ventricular (LV) systolic volume index (OR=1.034; CI: 1.005–1.062, p=0.019), LV diastolic volume index (OR=1.029; CI: 1.002–1.056, p=0.038), presence of hypersignal in T2 (OR=11.325; CI: 2.247–57.075, p=0.003), presence of late anteroseptal enhancement (OR=0.160; CI: 0.037–0.685, p=0.014), basal anteroseptal (OR=0.255; CI: 0.071–0.914, p=0.036) and lateral apical (OR=5.902; CI: 1.236–28.187, p=0.026). In relation to the increase in LVEF, significant differences were found in CMR in the following characteristics evaluated: LVEF (OR=0.870; CI: 0.758–0.988, p=0.047), end systolic volume of the right ventricle (OR=1.047; CI: 1.001–1.096, p=0.047), LV systolic diameter (OR=1.283; CI: 1.034–1.593, p=0.023), LV diastolic diameter (OR=1.225; CI: 1.012–1.482, p=0.038), LV systolic volume index (OR=1.340; CI: 1.066–1.685, p=0.012), LV diastolic volume index (OR=1.111; CI: 1.017–1.213, p=0.019) and right ventricular systolic volume index (OR=1.116; CI: 1.006–1.236, p=0.037). Conclusion We observed a significant association between combined events in the long-term follow-up with initial LVEF, LV systolic and diastolic volume indexes, T2 hypersignal and the presence of mid and basal anteroseptal and lateral apical late enhancement. Already related to the increase in LVEF in evolutionary CMR, we observed a significant association with initial LVEF, end systolic volume of the right ventricle, LV systolic and diastolic diameters, LV systolic and diastolic volume indexes and right ventricle systolic volume index. FUNDunding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): FAPESP

scholarly journals Ventricular Myocardial Sheet

2018 ◽  
Vol 14 (1) ◽  
pp. 50-57
Author(s):  
Mostafa R. Ali
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Muscle Fibers ◽  
Single Layer ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Ventricular Wall ◽  
Myocardial Layers ◽  
Running Pattern ◽  
The Right

Background: Despite the fact that the exact architecture and orientation of ventricular myocardium are critical to cardiac functions either in health or disease, it is still debated. Objectives: Anatomical demonstration of the ventricle myocardium (VM)as a single, long and continuous muscular sheet and this muscular sheet can be dived into 3-segments. As a new anatomical concept the left ventricle is a triple layers wall; whether the right ventricle is a single layer wall.Histological demonstration of different directions of muscle-fibers at each layer of ventricular myocardium. Type of the study: Cross- sectional study. Methods: In this study 100-heart (fish, chicken, goat, sheep and cow) were dissected and analyzed. Dental lacrona and wax knife used majorly in the dissection, boiling of the hearts with distilled water and finally opening them by the “opening-technique”. Results: Ventricular myocardium is a single, long and continuous muscular sheet in 100-samples of different species which had been included in the study (passing from the fish toward the cow). VMS can be divided into 3-segments in (100% of cow, 95% of goat and 85% of sheep). The left ventricle is a triple layers wall; whether the right ventricle is single layer wall, this result observed in (100% of cow, 95% of goat and 85% of sheep).Finally different directions of muscle fibers observed at each layer of ventricular myocardium where the subendocardial layer shows transverse running pattern of muscle fibers, mesocardial layer shows longitudinal running pattern of muscle fibers and subepicardial layer shows mixed running patterns of muscle fibers. Conclusion: Ventricular myocardium is single, long and continuous muscular sheet. This sheet consists of 3-segments. These segments coils in spiral track and form the triple layers left ventricular wall and the single layer right ventricular wall. By histological examination of ventricular myocardial layers different directions of muscle fibers observed at each layer.

Difficulties in diagnosing the myocardial infarction of the left ventricle inferior wall involving the right ventricle

2021 ◽  
Vol 19 (1) ◽  
pp. 82-85
Author(s):  
S. D. Mayanskaya ◽  
◽  
A. A. Gilmanov ◽  
T. V. Rudneva ◽  
M. M. Mangusheva ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Left Ventricular ◽  
Inferior Wall ◽  
Jugular Veins ◽  
St Segment Elevation ◽  
St Segment ◽  
The Right ◽  
Negative Predictor

The article presents a clinical observation of myocardial infarction (MI) of the inferior wall of the left ventricle (LV) with ST-segment elevation in combination with damage to the right ventricle (RV). Unfortunately, there is often a delay in the timely diagnosis of RV involvement in the process. This is because, at the beginning of the symptoms, it may not differ clinically from the typical manifestations of MI of the inferior-diaphragmatic region of the LV. However, the combination of LV inferior wall MI with RV MI is an important, negative predictor of increased mortality in these patients. In this case, RV MI was diagnosed after stenting of the right coronary artery, only when signs of hypotension and increased pressure of the jugular veins appeared. Based on the analysis of this clinical case, the authors discuss the need to record an ECG of the right heart in most patients with inferior MI, especially in the presence of hypotension without signs of acute left ventricular failure.

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