Cardiomyopathies and Heart Failure

Matsumori, Akira

doi:10.1007/978-1-4419-9264-2_1

Cited by 4 publications

(3 citation statements)

References 47 publications

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“…16) Elevations in various kinds of cytokines such as TNF-α, IL-6, and IL-1 have been reported in patients with CHF. [17][18][19] TNFR-I and II, the soluble TNF receptors, reflect the biological activity of TNF-α. One group has reported that TNFR-II is more predictive of the prognosis of CHF than TNF-α itself, 20) and Rauchhaus, et al 18) has found that TNFR-I correlates more closely with mortality than TNF-α in CHF patients.…”

Section: Discussionmentioning

confidence: 99%

<b>Relationship Between Exercise Intolerance and Levels of Neurohormonal Factors and Proinflammatory Cytokines in Patients With Stable Chronic Heart Failure</b>

et al. 2005

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SUMMARYWe investigated the correlations between exercise intolerance and the plasma levels of neurohormonal factors and proinflammatory cytokines in chronic heart failure (CHF) patients.Sixty-two CHF patients who underwent cardiopulmonary exercise testing (CPX) were enrolled in this study. Peak oxygen uptake (peak VO 2 ) and the plasma concentrations of noradrenaline (NA), brain natriuretic peptide (BNP), and soluble tumor necrosis factor receptors I and II (TNFR-I and -II) were all measured during the CPX. The patients were divided into three groups according to their peak VO 2 ; a severe exercise intolerance group (severe group; peak VO 2 < 18 mL/min/kg), moderate exercise intolerance group (moderate group; 18 ≤ peak VO 2 ≤ 24), and mild exercise intolerance group (mild group; peak VO 2 > 24).There were no significant differences in left ventricular ejection fraction (EF) among the three groups. NA and BNP both increased gradually in parallel with the worsening of exercise intolerance (NA, 211.5 ± 75.7 pg/mL, 331.8 ± 163.7, 441.9 ± 202.9, respectively; BNP, 37.9 ± 25.4 pg/mL, 148.9 ± 117.1, 247.9 ± 150.0, respectively). TNFR-I and II were significantly higher in the severe group than in the moderate group (1746.1 ± 950.7 versus 1085.2 ± 370.5 pg/mL and 2855.3 ± 1550.9 versus 2047.7 ± 648.7 pg/mL, respectively), while the values in the moderate group were not significantly different from those in the mild group. EF showed no significant correlations with NA, BNP, TNFR-I, or TNFR-II, whereas peak VO 2 exhibited significant negative correlations with NA (r = −0.50, P < 0.0001), BNP (r = −0.53, P < 0.0001), TNFR-I (r = −0.50, P < 0.0001), and TNFR-II (r = −0.45, P < 0.0001).It is concluded that NA and BNP rise in parallel with the degree of exercise intolerance, while TNFR-I and -II rise only when exercise intolerance reaches severe levels. (Int Heart J 2005; 46: 1049-1059

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Section: Discussionmentioning

confidence: 99%

<b>Relationship Between Exercise Intolerance and Levels of Neurohormonal Factors and Proinflammatory Cytokines in Patients With Stable Chronic Heart Failure</b>

et al. 2005

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“…14 Furthermore, some patients with myocarditis had repeated cycles of recurrence and remission. [14][15][16][17] It is presumed that upon viral infection, a persistent immune mechanism is activated, leading to a transition to dilated cardiomyopathy. [15][16][17] Moreover, potential persistent infection of the heart cannot be ruled out even after SARS-CoV-2 becomes undetectable on polymerase chain reaction of samples collected from the pharyngeal or nasal mucosa.…”

mentioning

confidence: 99%

“…[14][15][16][17] It is presumed that upon viral infection, a persistent immune mechanism is activated, leading to a transition to dilated cardiomyopathy. [15][16][17] Moreover, potential persistent infection of the heart cannot be ruled out even after SARS-CoV-2 becomes undetectable on polymerase chain reaction of samples collected from the pharyngeal or nasal mucosa. Therefore, for patients whose blood troponin levels are elevated after SARS-CoV-2 infection, long-term careful monitoring of cardiac function is necessary after recovery.…”

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confidence: 99%

Dilated Cardiomyopathy Risk in Patients with Coronavirus Disease 2019: How to Identify and Characterise it Early?

2020

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Multiple lines of evidence have shown that elevated blood troponin is strongly associated with poor prognosis in patients with the novel coronavirus disease 2019 (COVID-19). Possible mechanisms of myocardial injury in COVID-19 include ischaemia due to circulatory and respiratory failure, epicardial or intramyocardial small coronary artery thrombotic obstruction due to increased coagulability, and myocarditis caused by systemic inflammation or direct binding of the virus to its receptor, angiotensin-converting enzyme-2 (ACE2), which is abundantly expressed in the heart. It is postulated that persistent immune activation upon viral infection increases the risk of developing dilated cardiomyopathy in COVID-19 patients.

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Anti-inflammatory therapy for heart failure

Matsumori¹

2004

Current Opinion in Pharmacology

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Cardiomyopathies and Heart Failure

Cited by 4 publications

References 47 publications

<b>Relationship Between Exercise Intolerance and Levels of Neurohormonal Factors and Proinflammatory Cytokines in Patients With Stable Chronic Heart Failure</b>

<b>Relationship Between Exercise Intolerance and Levels of Neurohormonal Factors and Proinflammatory Cytokines in Patients With Stable Chronic Heart Failure</b>

Dilated Cardiomyopathy Risk in Patients with Coronavirus Disease 2019: How to Identify and Characterise it Early?

Anti-inflammatory therapy for heart failure

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