scholarly journals Low coronary perfusion pressure is associated with endocardial fibrosis in a rat model of volume overload cardiac hypertrophy

2004 ◽  
Vol 59 (5) ◽  
pp. 228-235 ◽  
Author(s):  
Maria Carolina Guido ◽  
Márcia Kiyomi Koike ◽  
Clovis de Carvalho Frimm
Keyword(s):  
Myocardial Fibrosis ◽  
Perfusion Pressure ◽  
Volume Fraction ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Volume Overload ◽  
Left Ventricular ◽  
Driving Pressure ◽  
Coronary Perfusion ◽  
Aortocaval Fistula

Left ventricular hypertrophy following volume overload is regarded as an example of cardiac remodeling without increased fibrosis accumulation. However, infarction is associated with increased fibrosis within the noninfarcted, hypertrophied myocardium, particularly in the subendocardial regions. It is conceivable to suppose that, as also occurs postinfarction, low coronary driving pressure may also interfere with accumulation of myocardial fibrosis following aortocaval fistula. PURPOSE: To investigate the role of acute hemodynamic changes in subsequent deposition of cardiac fibrosis in response to aortocaval fistula. METHOD: Aortocaval fistula were created in 4 groups of Wistar rats that were followed over 4 and 8 weeks: aortocaval fistula 4 and aortocaval fistula 8 (10 rats each) and their respective controls (sham-operated controls - Sh), Sh4 and Sh8 (8 rats each). Hemodynamic measurements were performed 1 week after surgery. Hypertrophy and fibrosis were quantified by myocyte diameter and collagen volume fraction at the end of follow up. RESULT: Compared with Sh4 and Sh8, pulse pressure, left ventricular end-diastolic pressure, and +dP/dt were higher in aortocaval fistula 4 and aortocaval fistula 8, but -dP/dt was similar. Coronary driving pressure (mm Hg), used as an estimate of perfusion pressure, was lower in aortocaval fistula 8 (52.6 ± 4.1) than in Sh8 (100.8 ± 1.3), but comparable between aortocaval fistula 4 (50.0 ± 8.9) and Sh4 (84.8 ± 2.3). Myocyte diameter was greater in aortocaval fistula 8, whereas interstitial and subendocardial fibrosis were greater in aortocaval fistula 4 and aortocaval fistula 8. Coronary driving pressure correlated inversely and independently with subendocardial fibrosis (r² = .86, P <.001), whereas left ventricular systolic pressure (r² = 0.73, P = .004) and end-diastolic pressure (r² = 0.55, P = 012) correlated positively and independently with interstitial fibrosis. CONCLUSION: Coronary driving pressure falls and ventricular pressures increase early after aortocaval fistula and are associated with subsequent myocardial fibrosis deposition.

Activation of PKC decreases myocardial O2consumption and increases contractile efficiency in rats

2001 ◽  
Vol 281 (5) ◽  
pp. H2191-H2197 ◽  
Author(s):  
Teruo Noguchi ◽  
Zengyi Chen ◽  
Stephen P. Bell ◽  
Lori Nyland ◽  
Martin M. LeWinter
Keyword(s):  
Perfusion Pressure ◽  
Diastolic Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Regulatory Proteins ◽  
Basal Metabolism ◽  
Coronary Perfusion ◽  
Kinase C ◽  
Rat Hearts ◽  
Pkc Activation

The effect of protein kinase C (PKC) activation on cardiac mechanoenergetics is not fully understood. To address this issue, we determined the effects of the PKC activator phorbol 12-myristate 13-acetate (PMA) on isolated rat hearts. Hearts were exposed to PMA with or without pretreatment with the PKC inhibitor chelerythrine. Contractile efficiency was assessed as the reciprocal of the slope of the linear myocardial O2consumption (V˙o 2) pressure-volume area (PVA) relation. PMA decreased contractility ( E max; −30 ± 8%; P < 0.05) and increased coronary perfusion pressure (+58 ± 11%; P < 0.01) without altering left ventricular end-diastolic pressure. Concomitantly, PMA decreased PVA-independentV˙o 2 [nonmechanical energy expenditure for excitation-contraction (E-C) coupling and basal metabolism] by 28 ± 8% ( P < 0.05) and markedly increased contractile efficiency (+41 ± 8%; P < 0.05) in a manner independent of the coronary vascular resistance. Basal metabolism was not affected by PMA. Chelerythrine abolished the PMA-induced vasoconstriction, negative inotropy, decreased PVA-independent V˙o 2, and increased contractile efficiency. We conclude that PKC-mediated phosphorylation of regulatory proteins reduces V˙o 2 via effects on both the contractile machinery and the E-C coupling.

scholarly journals Ginsenoside Re Improves Isoproterenol-Induced Myocardial Fibrosis and Heart Failure in Rats

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Quan-wei Wang ◽  
Xiao-feng Yu ◽  
Hua-li Xu ◽  
Xue-zhong Zhao ◽  
Da-yuan Sui
Keyword(s):  
Heart Failure ◽  
Myocardial Fibrosis ◽  
Group Treatment ◽  
Transforming Growth Factor ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Heart Weight ◽  
Hydroxyproline Content ◽  
Ginsenoside Re

Objective. Panax ginseng is used widely for treatment of cardiovascular disorders in China. Ginsenoside Re is the main chemical component of P. ginseng. We aimed to investigate the protective effect of ginsenoside Re on isoproterenol-induced myocardial fibrosis and heart failure in rats. Methods. A model of myocardial fibrosis and heart failure was established by once-daily subcutaneous injection of isoproterenol (5 mg/kg/day) to rats for 7 days. Simultaneously, rats were orally administrated ginsenoside Re (5 or 20 mg/kg) or vehicle daily for 4 weeks. Results. Isoproterenol enhanced the heart weight, myocardial fibrosis, and hydroxyproline content in rat hearts. Ginsenoside Re inhibited (at least in part) the isoproterenol-induced increase in heart weight, myocardial fibrosis, and hydroxyproline content. Compared with the isoproterenol group, treatment with ginsenoside Re ameliorated changes in left ventricular systolic pressure, left ventricular end diastolic pressure, and the positive and negative maximal values of the first derivative of left ventricular pressure. Ginsenoside Re administration also resulted in decreased expression of transforming growth factor (TGF)-β1 in serum and decreased expression of Smad3 and collagen I in heart tissue. Conclusion. Ginsenoside Re can improve isoproterenol-induced myocardial fibrosis and heart failure by regulation of the TGF-β1/Smad3 pathway.

Role of autoregulation in spatial and temporal perfusion heterogeneity of canine myocardium

1978 ◽  
Vol 235 (1) ◽  
pp. H64-H71 ◽  
Author(s):  
F. J. Sestier ◽  
R. R. Mildenberger ◽  
G. A. Klassen
Keyword(s):  
Spatial Heterogeneity ◽  
Perfusion Pressure ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Ventricular Myocardium ◽  
Small Region ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Temporal Heterogeneity ◽  
Ventricular Systolic Pressure

Spatial heterogeneity, the region-to-region variation in flow at an instant, and temporal heterogeneity, the time variation of flow in a small region of myocardium, were investigated with radioactive labeled microspheres in 111 regions of left ventricular myocardium. The error of the method was measured by simultaneously injecting four differently labeled microspheres (15 +/- 5 (SD) micron). The coefficient of variation (CV) was 6.5 +/- 1.0%. Spatial variation with autoregulation intact was 21.7 +/- 1.4% (CV); with autoregulation abolished and low perfusion pressure, it was 34.3 +/- 3.7%; and with normal perfusion pressure, 30.8 +/- 6.4% (differences not significantly). This degree of variation was similar in the entire left ventricle and its layers. Forces which tended to cause vessel closure (low perfusion pressure, ventricular systolic pressure, and ventricular diastolic pressure) tended to increase CV. Temporal heterogeneity as measured by 20-s intervals between microsphere injections was 11.1 +/- 1.0% (CV) with autoregulation, 9.8 +/- 1.3% (P less than 0.05) with autoregulation abolished, and 8.4 +/- 0.8% (P less than 0.05) when perfusion pressure was restored. A periodicity of flow cycles of 30-90 s was suggested by the data. These results suggest that spatial heterogeneity is less influenced by autoregulation than by hydraulic considerations, whereas temporal heterogeneity is a component of autoregulation.

Abstract 30: Incomplete Chest Recoil During Piglet CPR Worsens Hemodynamics

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Mathias Zuercher ◽  
Ronald W Hilwig ◽  
Jon Nysaether ◽  
Vinay M Nadkarni ◽  
Marc D Berg ◽  
...  
Keyword(s):  
Blood Flow ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Right Atrial ◽  
Coronary Perfusion ◽  
Parametric Data ◽  
Wilcoxon Rank Sum Test ◽  
The Right

Background : Incomplete chest recoil during cardiopulmonary resuscitation (CPR) (ie, leaning on the chest during the decompression phase) is purported to decrease venous return, and thereby decrease forward blood flow. Aim To determine the effect of 10% and 20% lean on hemodynamics during piglet CPR. Methods : 10 piglets (10.7±1.2 kg) were anesthetized with isoflurane and instrumented with micromanometer-tipped catheters in the right atrium (RA) and aorta (Ao). After induction of ventricular fibrillation, CPR was provided in three-minute epochs with no lean, 10% lean, or 20% lean while aortic systolic pressure (AoS) was targeted at 80–90 mmHg. Because the mean force to attain 80 –90 mm Hg AoS was 18 kg in preliminary studies, 10% and 20% lean were provided as 1.8 and 3.6 kg weights on the chest, respectively. Left ventricular myocardial blood flow (MBF) and cardiac index (CI) were determined by fluorescent, color-microsphere technique. Statistics: paired t -test and repeated measurement ANOVA for parametric, Wilcoxon Rank Sum Test and Friedman’s ANOVA for non-parametric data. Results : 10% and 20% lean resulted in higher right atrial diastolic pressure (RAD) and lower coronary perfusion pressure (CPP) than no lean. Hemodynamics were not different with 10% lean vs. 20% lean. Mean 10%–20% lean resulted in substantially lower MBF and CI than no lean (Table ). Conclusions : 10–20% leaning during CPR increases RAD, decreases CPP, and substantially decreases MBF and CI. Table

Nonischemic myocardial damage induced by nonocclusive constriction of coronary artery in rats

1991 ◽  
Vol 260 (3) ◽  
pp. H651-H661 ◽  
Author(s):  
J. M. Capasso ◽  
P. Li ◽  
P. Anversa
Keyword(s):  
Coronary Artery ◽  
Volume Fraction ◽  
Diastolic Pressure ◽  
Peripheral Resistance ◽  
Systolic Pressure ◽  
Myocardial Damage ◽  
Cellular Damage ◽  
Coronary Perfusion ◽  
Cross Sectional ◽  
Luminal Diameter

To determine whether reduction in coronary vessel diameter leads to alterations in cardiac function, coronary perfusion, and tissue integrity, the left coronary artery of rats was narrowed and ventricular hemodynamics measured at 3 and 5 days after surgery. Coronary artery narrowing averaged 62% and end-diastolic pressure was increased, whereas peak systolic pressure, positive change in pressure over time, stroke volume, and total peripheral resistance were decreased. However, this impairment of function was accompanied by a preservation of resting coronary blood flow (CBF), although a 43% decrease in maximal CBF was detected. Foci of reparative fibrosis and myocytolytic necrosis were found primarily in the endomyocardium and midmyocardium. These lesions were temporally distinct, corresponding to 5 days and 12- to 24-h-old forms of myocardial damage, respectively. The changes in maximal CBF correlated with the degree of stenosis, whereas the volume fraction, average cross-sectional area, and number of foci of reparative fibrosis lesions per unit area of myocardium correlated exclusively with end-diastolic pressure. In conclusion, reductions in luminal diameter of a major coronary artery not affecting resting coronary perfusion have a profound detrimental impact on cardiac performance and initiate immediate myocyte cell loss that is ongoing. Thus tissue and cellular damage may not be ischemic in nature but rather mediated by other mechanisms such as unbearable mechanical stress.

Mechanosensitive cardiac C-fiber response to changes in left ventricular filling, coronary perfusion pressure, hemorrhage, and volume expansion in rats

2005 ◽  
Vol 288 (2) ◽  
pp. H541-H552 ◽  
Author(s):  
Tilmann Ditting ◽  
Karl F. Hilgers ◽  
Karie E. Scrogin ◽  
Alexander Stetter ◽  
Peter Linz ◽  
...  
Keyword(s):  
Volume Expansion ◽  
Perfusion Pressure ◽  
Diastolic Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Coronary Perfusion ◽  
Sprague Dawley ◽  
Caval Vein ◽  
C Fibers ◽  
C Fiber

Left ventricular (LV) end-diastolic pressure (LVEDP) increase due to volume expansion (VExp) enhances mechanosensitive vagal cardiac afferent C-fiber activity (CNFA), thus decreasing renal sympathetic nerve activity (RSNA). Hypotensive hemorrhage (hHem) attenuates RSNA despite decreased LVEDP. We hypothesized that CNFA increases with any change in LVEDP. Coronary perfusion pressure (CPP), supposedly affected in both conditions, might also be a stimulus of CNFA. VExp and hHem were performed in anesthetized male Sprague-Dawley rats while blood pressure, heart rate, and RSNA were measured. Cervical vagotomy abolished RSNA response in both reflex responses. Single-unit CNFA was recorded while LVEDP was changed. Rapid changes (± 4, ±6, ±8 mmHg) were obtained by graded occlusion of the caval vein and descending aorta. Prolonged changes were obtained by VExp and hHem. Furthermore, CNFA was recorded in a modified Langendorff heart while CPP was changed (70, 100, 40 mmHg). Rapid LVEDP changes increased CNFA [caval vein occlusion: +16 ± 3 Hz (approximately +602%); aortic occlusion: +15 ± 3 Hz (approximately +553%); 70 units; P < 0.05]. VExp and hHem ( n = 6) increased CNFA [VExp: +10 ± 4 Hz (approximately +1,033%); hHem: +10 ± 2 Hz (approximately +1,225%); P < 0.05]. An increase in CPP increased CNFA [+2 ± 1 Hz (approximately +225%); P < 0.05], whereas a decrease in CPP decreased CNFA [−0.8 ± 0.4 Hz (approximately −50%); P < 0.05]. All C fibers recorded originated from the LV. CNFA increased with any LVEDP change but changed equidirectionally with CPP. Thus neither LVEDP nor CPP fully accounts directly for afferent C-fiber and reflex sympathetic responses. The intrinsic afferent stimuli and receptive fields accounting for reflex sympathoinhibition still remain cryptic.

Contribution of extravascular compression to reduction of maximal coronary blood flow

1992 ◽  
Vol 262 (1) ◽  
pp. H68-H77
Author(s):  
F. L. Abel ◽  
R. R. Zhao ◽  
R. F. Bond
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Perfusion Pressure ◽  
Left Ventricular Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Coronary Perfusion ◽  
Storage Site

Effects of ventricular compression on maximally dilated left circumflex coronary blood flow were investigated in seven mongrel dogs under pentobarbital anesthesia. The left circumflex artery was perfused with the animals' own blood at a constant pressure (63 mmHg) while left ventricular pressure was experimentally altered. Adenosine was infused to produce maximal vasodilation, verified by the hyperemic response to coronary occlusion. Alterations of peak left ventricular pressure from 50 to 250 mmHg resulted in a linear decrease in total circumflex flow of 1.10 ml.min-1 x 100 g heart wt-1 for each 10 mmHg of peak ventricular to coronary perfusion pressure gradient; a 2.6% decrease from control levels. Similar slopes were obtained for systolic and diastolic flows as for total mean flow, implying equal compressive forces in systole as in diastole. Increases in left ventricular end-diastolic pressure accounted for 29% of the flow changes associated with an increase in peak ventricular pressure. Doubling circumferential wall tension had a minimal effect on total circumflex flow. When the slopes were extrapolated to zero, assuming linearity, a peak left ventricular pressure of 385 mmHg greater than coronary perfusion pressure would be required to reduce coronary flow to zero. The experiments were repeated in five additional animals but at different perfusion pressures from 40 to 160 mmHg. Higher perfusion pressures gave similar results but with even less effect of ventricular pressure on coronary flow or coronary conductance. These results argue for an active storage site for systolic arterial flow in the dilated coronary system.

scholarly journals Cardiac arrest complicating cardiogenic shock: from pathophysiological insights to Impella-assisted cardiopulmonary resuscitation in a pheochromocytoma-induced Takotsubo cardiomyopathy—a case report

2021 ◽  
Vol 5 (3) ◽  
Author(s):  
Filippo Zilio ◽  
Simone Muraglia ◽  
Roberto Bonmassari
Keyword(s):  
Cardiac Arrest ◽  
Cardiopulmonary Resuscitation ◽  
Left Ventricle ◽  
Cardiogenic Shock ◽  
Takotsubo Cardiomyopathy ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Coronary Perfusion ◽  
Refractory Cardiac Arrest

Abstract Background A ‘catecholamine storm’ in a case of pheochromocytoma can lead to a transient left ventricular dysfunction similar to Takotsubo cardiomyopathy. A cardiogenic shock can thus develop, with high left ventricular end-diastolic pressure and a reduction in coronary perfusion pressure. This scenario can ultimately lead to a cardiac arrest, in which unloading the left ventricle with a peripheral left ventricular assist device (Impella®) could help in achieving the return of spontaneous circulation (ROSC). Case summary A patient affected by Takotsubo cardiomyopathy caused by a pheochromocytoma presented with cardiogenic shock that finally evolved into refractory cardiac arrest. Cardiopulmonary resuscitation was performed but ROSC was achieved only after Impella® placement. Discussion In the clinical scenario of Takotsubo cardiomyopathy due to pheochromocytoma, when cardiogenic shock develops treatment is difficult because exogenous catecholamines, required to maintain organ perfusion, could exacerbate hypertension and deteriorate the cardiomyopathy. Moreover, as the coronary perfusion pressure is critically reduced, refractory cardiac arrest could develop. Although veno-arterial extra-corporeal membrane oxygenation (va-ECMO) has been advocated as the treatment of choice for in-hospital refractory cardiac arrest, in the presence of left ventricular overload a device like Impella®, which carries fewer complications as compared to ECMO, could be effective in obtaining the ROSC by unloading the left ventricle.

scholarly journals The link between left ventricular extracellular volume determined by T1 myocardial mapping and gut microbiota composition in individuals with heart failure and preserved ejection fraction

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
A.N Kaburova ◽  
O.M Drapkina ◽  
S.M Uydin ◽  
M.V Vishnyakova ◽  
M.S Pokrovskaya ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Gut Microbiota ◽  
Myocardial Fibrosis ◽  
Volume Fraction ◽  
Extracellular Volume ◽  
Left Ventricular ◽  
Diffuse Myocardial Fibrosis ◽  
Rrna Gene ◽  
Preserved Ejection Fraction

Abstract Introduction Heart failure with preserved ejection fraction (HFpEF) represents a major challenge in modern cardiology. As described previously, in HFpEF comorbidities promote a systemic inflammatory state, leading to diffuse myocardial fibrosis resulting in myocardial stiffening. Gut dysbiosis which is considered as the novel source of chronic systemic inflammation has been actively investigated as the risk factor for the development and aggravation of cardiovascular diseases including heart failure. Cardiac magnetic resonance T1-mapping is a novel tool, which allows noninvasive quantification of the extracellular space and diffuse myocardial fibrosis. Moreover, the extracellular volume (ECV) fraction can be calculated, providing information on the relative expansion of the extracellular matrix, thus being a noninvasive alternative to myocardial biopsy studies. Purpose The research was aimed at investigating the correlation between the left ventricular ECV and gut microbial genera in patients with HFpEF. Methods 42 patients with confirmed HF-pEF (mediana and interquartile range of age 67 [64; 72] years, 47% men, body mass index &lt;35 kg/m2 with no history of myocardial infarction or diabetes mellitus) were enrolled in the study. The patients underwent transthoracic echocardiography with Doppler study, HF-pEF was confirmed according to the recent ESC guidelines (based on E/e' ratio, N-terminal pro-B type natriuretic peptide &gt;125 pg/ml and symptoms of heart failure). The intestinal microbiome was investigated using high-throughput sequencing of bacterial 16S rRNA gene. As the last step of research T1-myocardial mapping with the modified look-locker inversion-recovery protocol (MOLLI) sequence at 1.5 Tesla was performed to assess left ventricular extracellular volume fraction. Results The mean±std in ECV was 31.02±4.4%. The relative abundance (%) of the most prevalent phyla in gut microbiota was 48±22.5 for Firmicutes, 47.4±22.8 for Bacteroidetes and 1.5 [1.5; 2.5] for Proteobacteria. The analysis showed significant negative correlations between ECV and the following bacterial genera: Faecalibacterium (r=−0.35), Blautia (r=−0.43), Lachnoclostridium (r=−0.32). Moreover ECV positively correlated with Holdemania (r=0.4), Victivallis (r=0.38), Dehalobacterium (r=0.38), Enterococcus (r=0.33) and Catabacter (r=0.32). All correlation values with p&lt;0.05. Conclusion We discovered both negative and positive significant correlations between ECV – the non-invasive marker of myocardial fibrosis and several bacterial genera, which may have negative impact on myocardial remodeling in HF-pEF. Funding Acknowledgement Type of funding source: None

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