Mechanics of the left ventricular myocardial interstitium: effects of acute and chronic myocardial edema

Desai, Ketaki V.; Laine, Glen A.; Stewart, Randolph H.; Cox, Charles S.; Quick, Christopher M.; Allen, Steven J.; Fischer, Uwe

doi:10.1152/ajpheart.00860.2007

Cited by 91 publications

(73 citation statements)

References 45 publications

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“…The elevated LVMI in the AMC group (p = 0.034) results from acute inflammation with successive edema. Edema within the myocardium may result in capillary compression and reduced diastolic and systolic cardiac function [20,21]. We were able to identify wall motion abnormalities in 63 % of the AMC group, which can be broken down into regional distribution in 47 % and global distribution in 16 %.…”

Section: Functional Analysismentioning

confidence: 90%

Functional and Morphological Parameters with Tissue Characterization of Cardiovascular Magnetic Imaging in Clinically Verified “Infarct-like Myocarditis”

Schwab¹,

Rogg²,

Pauschinger³

et al. 2015

Fortschr Röntgenstr

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Purpose: Cardiac magnetic resonance (CMR) has increasingly proved to be a valuable diagnostic tool for evaluating patients with suspected myocarditis. The objective of this study was to evaluate the diagnostic value of functional and morphological parameters including tissue characterization in patients with ?infarct-like myocarditis?. Materials and Methods: 43 patients with clinically verified cases of ?infarct-like myocarditis? (median time to MRI scanning after admission for acute symptoms 3 days) and 35 control patients matched by age and sex were included in this retrospective case control study. In this study we used a 1.5?T MRI scanner conducting steady-state-free-precession sequences, T2-weighted imaging, T1-weighted imaging before and after contrast administration and late gadolinium enhancement sequences. According to the recommendations for CMR diagnosis of myocarditis (Lake Louise consensus criteria), a scan was positive for acute myocarditis if 2 of 3 CMR criteria were present. Results: 30?% of the patients with ?infarct-like myocarditis? had a reduced left ventricular ejection fraction, 11?% had an increased LV end-diastolic volume index and 35?% had an increased LV mass index. The sensitivity of wall motion abnormalities was 63?% with a regional distribution in 49?%. In 47?% of cases regional wall motion abnormalities were present in the lateral left ventricular segments. Pericardial effusions were discovered in 65?% of cases with a circular appearance in 21?% and focal manifestation in 44?%. The diagnostic sensitivity, specificity, and accuracy of CMR in patients with ?infarct-like myocarditis? were 67?%, 100?% and 82?%, respectively. The LGE alone was the most sensitive test parameter with 86?%, providing a specificity of 100?% and accuracy of 92?%. Conclusion: Our study results can be applied to the subgroup of patients with ?infarct-like myocarditis?, where we found that LGE alone was the most sensitive test parameter. In addition to tissue characterization, the functional and morphological analysis of patients with acute myocarditis provides a useful further diagnostic tool. Key Points: ??Infarct-like myocarditis can be diagnosed by CMR with high validity and reliability. ??LGE allone performed best with a sensitivity of 86?%. ??Functional and morphological CMR parameters in addition to tissue characterization are useful tool in the diagnosis of acute myocarditis. Citation Format: ??Schwab J, Rogg H-J, Pauschinger M et?al. Functional and Morphological Parameters with Tissue Characterization of Cardiovascular Magnetic Imaging in Clinically Verified ?Infarct-like Myocarditis?. Fortschr R?ntgenstr 2016; 188: 365???373

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Section: Functional Analysismentioning

confidence: 90%

Functional and Morphological Parameters with Tissue Characterization of Cardiovascular Magnetic Imaging in Clinically Verified “Infarct-like Myocarditis”

Schwab¹,

Rogg²,

Pauschinger³

et al. 2015

Fortschr Röntgenstr

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“…In addition, CPB has been associated with decreased myocardial systolic and diastolic function. The prevalence of generalized edema in neonates undergoing cardiovascular surgery with CPB has been reported to be 37% and 54% [4,5,41,42]. In our study, we found that the expression of cGMP and AQP1 were lowest at 6 h, and then began to increase, and reached peak levels at 48 h. Meanwhile, water content of myocardial tissue increased following the CPB surgery, and peaked at 48 h. These findings suggested that cGMP and AQP1 had important roles in water intake during CPB.…”

Section: Discussionmentioning

confidence: 99%

“…Conversely, the use of cardiopulmonary bypass (CPB) causes profound alterations in the homeostasis of physiological fluids, which often results in myocardial edema. CPB has been associated with decreased myocardial systolic and diastolic function [4,5]. However, none of these aspects of myocardial edema in CPB has been completely characterized.…”

Section: Introductionmentioning

confidence: 99%

The Role of Aquaporin 1 Activated by cGMP in Myocardial Edema Caused by Cardiopulmonary Bypass in Sheep

Ding

Yan

Bao

et al. 2013

Cell Physiol Biochem

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Background/Aims: Most cardiac procedures involve the use of cardiopulmonary bypass (CPB), which pumps oxygenated blood to the body while the heart and lungs are isolated. CPB can cause profound alterations V in the homeostasis of physiological fluids, which often results in myocardial edema. In our study, we used sheep CPB model of in vivo and in vitro to assess the relationship between cGMP and AQP1 during CPB. Methods: ODQ, a specific inhibitor of soluble guanylate cyclase (sGC), was used to treat the CPB animals or cardiomyocytes. Left ventricular function of each group was determined by pressure-volume system. Water content of myocardial tissue was assessed by dry-wet weight, and cardiomyocytes water permeability was also calculated. The concentration of cGMP was determined by Radioimmunoassay (RIA). mRNA and protein expression of AQP1 were detected by real-time PCR and western blot, respectively. Results: The relative expression level of AQP1 mRNA and protein at each time point (0, 6, 12, 24 or 48 h) after CPB was significantly increased (1.18-fold at 12 h, 1.77-fold at 24 h and 2.18-fold at 48h) compared with each sham group, the protein expression of AQP1 also showed a rising trend after CPB. The degree of myocardial edema (75.1% at 12 h, 79.3% at 24 h and 81.0% at 48h) increased following the CPB surgery. The mRNA expression level of AQP1 was significantly decreased by 39.7% (p<0.01) upon treatment with ODQ compared with the CPB-only group, and inhibition of cGMP pathway also can significantly decrease the degree of myocardial edema (84.7% in control group, while 75.2% in ODQ group) and improve cardiac function in sheep after CPB. Results of in vitro experiments showed the same changing trends as in vivo. Conclusion: cGMP pathway controls water channels and then affects water intake during CPB through an AQP1-mediated pathway.

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“…The resulting alveolar congestion and edema is in part mediated by altered expression of epithelial sodium channel and aquiporin-5 expression. Similar mechanisms may also contribute to myocardial interstitial edema and dysfunction [44]. Transgenic sickle mice subjected to renal IRI exhibited significantly increased myocardial capillary congestion, serum amyloid-P (murine equivalent of C-reaction protein), and renal expression of caspase-3 compared with controls [45].…”

Section: Pathophysiologic Mechanisms Of Aki-induced Cardiac Injurymentioning

confidence: 99%

“…In addition, fluid removal in these patients, either through loop diuretics use [55] or ultrafiltration [56], was associated with higher survival. Fluid accumulation may adversely impact myocardial performance [44], predispose to ventricular arrhythmias [57] and may contribute to maladaptive ventricular remodelling and myocardial fibrosis [44,58].…”

Section: Indirect Mechanismsmentioning

confidence: 99%

Cardiorenal Syndrome Type 3: Pathophysiologic and Epidemiologic Considerations

Bagshaw

Hoste

Braam

et al. 2013

Contributions to Nephrology

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Cardiorenal syndrome (CRS) type 3 is a subclassification of the CRS whereby an episode of acute kidney injury (AKI) precipitates and contributes to the development of acute cardiac injury. There is limited understanding of the pathophysiologic mechanisms of how AKI contributes to acute cardiac injury and/or dysfunction. An episode of AKI may have effects that depend on the severity and duration of AKI and that both directly and indirectly predispose to an acute cardiac event. Moreover, baseline susceptibility will modify the subsequent risk for cardiac events associated with AKI. Experimental data suggest cardiac injury may be directly induced by inflammatory mediators, oxidative stress, apoptosis and activation of neuroendocrine systems early after AKI. Likewise, AKI may be associated with physiologic derangements (i.e. volume overload; metabolic acidosis, retention of uremic toxins, hyperkalemia; hypocalcemia), alterations to coronary vasoreactivity, and ventricular remodeling and fibrosis that indirectly exert negative effects on cardiac function. AKI may also adversely impact cardiac function by contributing to alternations in drug pharmacokinetics and pharmacodynamics. Additional experimental and transla-

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Mechanics of the left ventricular myocardial interstitium: effects of acute and chronic myocardial edema

Cited by 91 publications

References 45 publications

Functional and Morphological Parameters with Tissue Characterization of Cardiovascular Magnetic Imaging in Clinically Verified “Infarct-like Myocarditis”

Functional and Morphological Parameters with Tissue Characterization of Cardiovascular Magnetic Imaging in Clinically Verified “Infarct-like Myocarditis”

The Role of Aquaporin 1 Activated by cGMP in Myocardial Edema Caused by Cardiopulmonary Bypass in Sheep

Cardiorenal Syndrome Type 3: Pathophysiologic and Epidemiologic Considerations

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