Protection of the Myocardium by Coronary Perfusion

1976 ◽  
pp. 57-63
Author(s):  
G. M. Rees
Keyword(s):  
Coronary Perfusion

Iron storage sites in the myocardium as revealed by cytohistochemistry

1988 ◽  
Vol 46 ◽  
pp. 394-395
Author(s):  
M. Ashraf ◽  
F. Thompson ◽  
S. Miki ◽  
P. Srivastava
Keyword(s):  
Cardiac Tissue ◽  
Coronary Perfusion ◽  
Intracellular Iron ◽  
Ether Anesthesia ◽  
Intense Staining ◽  
Iron Storage ◽  
Thin Sections ◽  
Rat Hearts ◽  
Cacodylate Buffer ◽  
Made In

Iron is believed to play an important role in the pathogenesis of ischemic injury. However, the sources of intracellular iron in myocytes are not yet defined. In this study we have attempted to localize iron at various cellular sites of the cardiac tissue with the ferrocyanide technique.Rat hearts were excised under ether anesthesia. They were fixed with coronary perfusion with 3% buffered glutaraldehyde made in 0.1 M cacodylate buffer pH 7.3. Sections, 60 μm in thickness, were cut on a vibratome and were incubated in the medium containing 500 mg of potassium ferrocyanide in 49.5 ml H2O and 0.5 ml concentrated HC1 for 30 minutes at room temperature. Following rinses in the buffer, tissues were dehydrated in ethanol and embedded in Spurr medium.The examination of thin sections revealed intense staining or reaction product in peroxisomes (Fig. 1).

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.

Functional assessment of myocardial ischemia by intracoronary electrocardiogram

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M.R Bigler ◽  
F Praz ◽  
G.C.M Siontis ◽  
M Stoller ◽  
R Grossenbacher ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Primary Study ◽  
Coronary Perfusion ◽  
Funding Source ◽  
Maximal Heart Rate ◽  
Fractional Flow ◽  
Coronary Syndrome ◽  
Flow Reserve ◽  
St Segment ◽  
Coronary Lesions

Abstract Background In patients with chronic coronary syndrome (CCS), percutaneous coronary intervention (PCI) targets hemodynamically significant stenoses, i.e., those thought to cause ischemia. The hemodynamic severity of a coronary stenosis increases with its tightness and with the myocardial mass of viable myocardium downstream of the stenosis. Besides the structural angiographic approach, assessment of functional relevance by pressure measurements (fractional flow reserve, FFR; instantaneous wave-free ratio, iFR) is recommended. However, visual angiographic assessment continues to dominate the treatment decisions for intermediate coronary lesions. Conversely, intracoronary ECG (icECG) potentially provides an inexpensive, sensitive and direct measure of myocardial ischemia. Purpose The goal of this study was to test the accuracy of intracoronary ECG during pharmacologic inotropic stress to determine coronary lesion severity in comparison to established physiologic indices (FFR/iFR) as well as with quantitatively determined percent diameter stenosis (%S) using biplane coronary angiography. Method This was a prospective, open-label study in patients with CCS. The primary study end point was the maximal change in icECG ST-segment shift during pharmacologic inotropic stress induced by dobutamine plus atropine obtained within 1 minute after the point of maximal heart rate (estimated by the formula 220 - age). IcECG was acquired by attaching an alligator clamp to the angioplasty guidewire positioned downstream of a stenosis. For the pressure-derived ratios, i.e. FFR and iFR, the coronary perfusion pressure downstream of a lesion as well as the aortic pressure were continuously recorded. Results One hundred patients were included in the study. Pearson-Correlation coefficient was significant between icECG and all three comparators (%S p<0.001, iFR p<0.001, FFR p<0.001). Using the FFR threshold of 0.80 defining coronary hemodynamic significance, ROC-analysis of the absolute icECG ST-segment shift showed an area under the curve (AUC) of 0.708±0.053 (p=0.0001, n=100, FFR<0.80 n=41). AUC for iFR was 0.919±0.030 (p<0.0001), for percent diameter stenosis it was 0.867±0.036 (p<0.0001). Conclusions During pharmacologic inotropic stress, intracoronary ECG ST-segment shift provides specific evidence for regional myocardial ischemia irrespective of the etiology and thus, provides an additional (patho-)physiologic information for decision making in borderline coronary lesions. Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): Swiss Heart Foundation

scholarly journals 3D ultrasound coronarography: first proof of concept study on isolated beating rat hearts

2021 ◽  
Vol 22 (Supplement_1) ◽  
Author(s):  
O Demeulenaere ◽  
P Mateo ◽  
P Sandoval ◽  
O Villemain ◽  
M Tanter ◽  
...  
Keyword(s):  
Contrast Agents ◽  
Flow Velocity ◽  
Coronary Flow ◽  
3D Ultrasound ◽  
Frame Rate ◽  
Doppler Imaging ◽  
Coronary Perfusion ◽  
Blood Flows ◽  
Flow Reserve ◽  
Rat Hearts

Abstract Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): Bettencourt Foundation Background/Introduction We demonstrated recently that Ultrafast ultrasound Doppler imaging can image the intramyocardial coronary circulation in beating hearts of large animals and patients [1]. Yet, ultrasound spatial resolution remains limited by wave physics and coronaries smaller than ∼100 µm could not be imaged. Ultrasound Localization Microscopy (ULM) [2] was recently introduced to tackle this issue and exploit the micrometric localization of microbubble contrast agents at ultrafast frame rate in order to image blood flows in micrometer vessels. Purpose The objective of this work was to demonstrate that 3D ultrafast ultrasound with contrast agents can provide the full 3D mapping of the coronary microcirculation with quantitative flow velocity on a beating rat heart. Methods Acquisitions were performed on ex vivo rat hearts (n = 5) with retrograde perfusion (Langendorff model). A flow of a Krebs–Henseleit solution mixed with a diluted microbubbles solution (0.22%) was perfused at controlled pressure into the coronary arteries (between 5 and 15 mL/min). We used a 32 × 32 elements, 8-MHz matrix-array ultrasound transducer connected to a 1024-channel programmable ultrasound scanner. An ultrafast Doppler imaging sequence consisting of 9 plane waves was transmitted at a PRF of 20 kHz during 270 ms and repeated 40 times. After beamforming and SVD clutter filtering, the microbubbles were localized and tracked in 3D. Flow velocity were mapped at baseline and after infusion of Adenosine (10e-5 µMol) at constant coronary perfusion pressure (120 mm Hg). Eventually, the hearts were fixed using formaldehyde perfusion and imaged by µCT after injection of radio opaque agent. Results We successfully imaged the coronary blood flows of entire rat hearts. It revealed the entire vasculature from large main coronaries arteries (cross section up to 1 mm) to small arterioles (smaller than 40 µm). Coronary flow velocities ranged from [1 – 50] cm/s depending on the arteries diameter. Velocity estimates were validated in vitro in tubes of Ø0.58mm and were in good agreement with theoretical values of a Poiseuille’s flow (relative ratio of 10% for maximum velocities). After Adenosine infusion, perfusion flow rates increased 102% ± 50% (p < 0.05) on average. Eventually, anatomy revealed by 3D ultrasound coronarography was in accordance with the anatomy revealed by the µCT. Conclusion(s) We demonstrated the feasibility of 3D ultrasound coronarography on isolated beating rat hearts. This technique has the potential to become a novel imaging tool to investigate the coronary micro-circulation and quantify non-invasively the Coronary Flow Reserve (CFR). Abstract Figure. Ultrasound coronarography

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 Esmolol during cardiopulmonary resuscitation reduces neurological injury in a porcine model of cardiac arrest

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Laura Ruggeri ◽  
Francesca Nespoli ◽  
Giuseppe Ristagno ◽  
Francesca Fumagalli ◽  
Antonio Boccardo ◽  
...  
Keyword(s):  
Cardiopulmonary Resuscitation ◽  
Porcine Model ◽  
Neuronal Degeneration ◽  
Neuron Specific Enolase ◽  
Coronary Perfusion Pressure ◽  
Neurological Injury ◽  
Saline Control ◽  
Preclinical Model ◽  
Coronary Perfusion ◽  
To Receive

AbstractPrimary vasopressor efficacy of epinephrine during cardiopulmonary resuscitation (CPR) is due to its α-adrenergic effects. However, epinephrine plays β1-adrenergic actions, which increasing myocardial oxygen consumption may lead to refractory ventricular fibrillation (VF) and poor outcome. Effects of a single dose of esmolol in addition to epinephrine during CPR were investigated in a porcine model of VF with an underlying acute myocardial infarction. VF was ischemically induced in 16 pigs and left untreated for 12 min. During CPR, animals were randomized to receive epinephrine (30 µg/kg) with either esmolol (0.5 mg/kg) or saline (control). Pigs were then observed up to 96 h. Coronary perfusion pressure increased during CPR in the esmolol group compared to control (47 ± 21 vs. 24 ± 10 mmHg at min 5, p < 0.05). In both groups, 7 animals were successfully resuscitated and 4 survived up to 96 h. No significant differences were observed between groups in the total number of defibrillations delivered prior to final resuscitation. Brain histology demonstrated reductions in cortical neuronal degeneration/necrosis (score 0.3 ± 0.5 vs. 1.3 ± 0.5, p < 0.05) and hippocampal microglial activation (6 ± 3 vs. 22 ± 4%, p < 0.01) in the esmolol group compared to control. Lower circulating levels of neuron specific enolase were measured in esmolol animals compared to controls (2[1–3] vs. 21[16–52] ng/mL, p < 0.01). In this preclinical model, β1-blockade during CPR did not facilitate VF termination but provided neuroprotection.

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