Coronary venous therapy to improve microvascular dysfunction

2021 ◽  
pp. 1-5
Author(s):  
T. Gori
Keyword(s):  
Coronary Circulation ◽  
Venous Pressure ◽  
Microvascular Disease ◽  
Microvascular Dysfunction ◽  
Diagnostic Tools ◽  
Coronary Perfusion ◽  
Venous Circulation ◽  
Coronary Syndromes ◽  
Invasive Techniques

The coronary circulation is a complex system in which vascular resistances are determined by an interplay of forces in at least three compartments: the epicardial, the microvascular, and the venous district. Cardiologists, and particularly interventional cardiologists, normallly place the focus of their attention on diseases of the epicardial coronary circulation as possible causes of coronary syndromes and neglect the importance of the other two compartments of coronary circulation. The study of the coronary microcirculation, an increasingly recognized source of ischemia, has long been disregarded, but is witnessing a revival since the (re-)introduction of diagnostic tools in the better equipped catheterization laboratories. Unfortunately, to date our understanding of coronary microvascular disease remains incomplete and the numerous proposed classifications fail to reflect its complexity. Further, no specific therapy for these disorders is available. The coronary venous circulation is an even more neglected third vascular district. Its role in regulating coronary resistances is almost completely unexplored, but inital evidence suggests that the modulation of venous pressure might help improve coronary perfusion. Coronary sinus interventions are a group of invasive techniques (both surgical and catheter-based) that are designed to treat ischaemic heart disease by increasing coronary venous pressure and therefore redistributing coronary blood flow towards the endocardium. In this review paper, we revise the role of these interventions with particular focus on acute and chronic coronary microvascular disease.

scholarly journals Assessment and pathophysiology of microvascular disease: recent progress and clinical implications

2020 ◽  
Author(s):  
Stefano Masi ◽  
Damiano Rizzoni ◽  
Stefano Taddei ◽  
Robert Jay Widmer ◽  
Augusto C Montezano ◽  
...  
Keyword(s):  
Ex Vivo ◽  
Diagnostic Testing ◽  
Microvascular Disease ◽  
Microvascular Dysfunction ◽  
Microvascular Changes ◽  
Increased Risk ◽  
Technical Advances ◽  
Cv Disease ◽  
Invasive Techniques

Abstract The development of novel, non-invasive techniques and standardization of protocols to assess microvascular dysfunction have elucidated the key role of microvascular changes in the evolution of cardiovascular (CV) damage, and their capacity to predict an increased risk of adverse events. These technical advances parallel with the development of novel biological assays that enabled the ex vivo identification of pathways promoting microvascular dysfunction, providing novel potential treatment targets for preventing cerebral-CV disease. In this article, we provide an update of diagnostic testing strategies to detect and characterize microvascular dysfunction and suggestions on how to standardize and maximize the information obtained from each microvascular assay. We examine emerging data highlighting the significance of microvascular dysfunction in the development CV disease manifestations. Finally, we summarize the pathophysiology of microvascular dysfunction emphasizing the role of oxidative stress and its regulation by epigenetic mechanisms, which might represent potential targets for novel interventions beyond conventional approaches, representing a new frontier in CV disease reduction.

scholarly journals GPER modulates tone and coronary vascular reactivity in male and female rats

2017 ◽  
Vol 59 (2) ◽  
pp. 171-180 ◽  
Author(s):  
Angelina Rafaela Debortoli ◽  
Wender do Nascimento Rouver ◽  
Nathalie Tristão Banhos Delgado ◽  
Vinicius Mengal ◽  
Erick Roberto Gonçalves Claudio ◽  
...  
Keyword(s):  
Protein Expression ◽  
Vascular Reactivity ◽  
Coronary Circulation ◽  
Superoxide Production ◽  
Female Rats ◽  
Male Rats ◽  
Coronary Perfusion ◽  
Dependent Manner ◽  
Coronary Tone

Compared with age-matched men, premenopausal women are largely protected from coronary artery disease, a difference that is lost after menopause. The effects of oestrogens are mediated by the activation of nuclear receptors (ERα and ERβ) and by the G protein-coupled oestrogen receptor (GPER). This study aims to evaluate the potential role of GPER in coronary circulation in female and male rats. The baseline coronary perfusion pressure (CPP) and the concentration–response curve with a GPER agonist (G-1) were evaluated in isolated hearts before and after the blockade of GPER. GPER, superoxide dismutase (SOD-2), catalase and gp91phox protein expression were assessed by Western blotting. Superoxide production was evaluated ‘in situ’ via dihydroethidium fluorescence (DHE). GPER blockade significantly increased the CPP in both groups, demonstrating the modulation of coronary tone by GPER. G-1 causes relaxation of the coronary bed in a concentration-dependent manner and was significantly higher in female rats. No differences were detected in GPER, SOD-2 and catalase protein expression. However, gp91phox expression and DHE fluorescence were higher in male rats, indicating elevated superoxide production. Therefore, GPER plays an important role in modulating coronary tone and reactivity in female and male rats. The observed differences in vascular reactivity may be related to the higher superoxide production in male rats. These findings help to elucidate the role of GPER-modulating coronary circulation, providing new information to develop a potential therapeutic target for the treatment of coronary heart disease.

Effects of venous pressure on coronary circulation and intramyocardial fluid mechanics

1994 ◽  
Vol 267 (3) ◽  
pp. H1002-H1009 ◽  
Author(s):  
I. Izrailtyan ◽  
H. F. Frasch ◽  
J. Y. Kresh
Keyword(s):  
Coronary Flow ◽  
Coronary Circulation ◽  
Venous Pressure ◽  
Rabbit Heart ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Right Heart ◽  
Tissue Pressure ◽  
Parallel Shift ◽  
The Right

This investigation examined the interaction between right heart pressure (RHP), coronary perfusion pressure (CPP), intramyocardial tissue pressure (IMP), and coronary flow mechanics, including partitioning of coronary effluent in the isolated Krebs-Henseleit perfused rabbit heart. The major new finding was a parallel shift in the IMP-inflow relationship to a higher tissue pressure level in response to an increase in RHP. Accompanying the rise in RHP from 0 to 15 and 25 mmHg, IMP at zero coronary inflow in the beating (and arrested) heart increased from 5.8 +/- 1.0 (7.7 +/- 1.2) to 16.3 +/- 1.2 (17.9 +/- 1.3) and 28.6 +/- 1.7 (26.4 +/- 2.0) mmHg, respectively. A concomitant parallel shift in the CPP-inflow relation to higher pressures was consistently observed. The fraction of total coronary flow drained by the right heart was not constant. A higher partition of coronary outflow to the left heart (7.8 +/- 3.8, 34.3 +/- 3.0, and 47.9 +/- 4.3%, respectively) accompanied the increase in RHP. Intramyocardial partitioning of coronary outflow pathways mediates the effects of venous pressure modulation on coronary circulation. The interaction between coronary venous pressure and the extravascular environment modifies the effective back pressure to arterial inflow.

Abstract 149: Role of Pre and Intra-Arrest Hemodynamics in Evolution of the Ventricular Fibrillation Electrocardiogram Waveform

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_2) ◽  
Author(s):  
Caelie E Kern ◽  
David D Salcido
Keyword(s):  
Ventricular Fibrillation ◽  
Trajectory Analysis ◽  
Venous Pressure ◽  
Coronary Perfusion Pressure ◽  
Spontaneous Circulation ◽  
Coronary Perfusion ◽  
Pressure Transducers ◽  
Surface Ecg ◽  
Electrical Induction

Purpose: Quantitative waveform measures (QWM) of the ventricular fibrillation (VF) waveform have been shown in laboratory and clinical studies to be predictive of return of spontaneous circulation (ROSC) and survival to hospital discharge. During resuscitation, QWM are responsive to hemodynamic changes resulting from CPR. It is not known whether the trajectory of QWM are affected by pre-arrest hemodynamics or intra-arrest arterio-venous pressure equilibration. We sought to investigate the role of hemodynamics on the evolution of VF before and during prolonged VF. Methods: We pooled data from six previous porcine experiments. Each modeled prolonged VF and included electrical induction of VF which was left untreated for up to 10 minutes, followed by attempted resuscitation. All animals were instrumented with pressure transducers (Millar, MikroTip) placed via femoral cutdown in the aorta and right atrium, as well as Lead II surface ECG. Signals were recorded continuously at 1000Hz with a data acquisition unit (PowerLab, ADInstruments). Mean baseline central arterial (CAP) and central venous pressure (CVP) were calculated from 1- minute of immediate pre-VF pressure traces. Coronary perfusion pressure (CPP) during untreated VF was calculated as the continuous difference between the CAP and CVP channels. Median slope (MS), a QWM, was calculated in 1-second windows and interpolated to the full length of the intra-arrest ECG. For trajectory analysis, CPP and MS traces were normalized on a 0-1 scale and grouped by morphological similarity. Pearson’s Correlation coefficient was calculated between corresponding CPP and MS traces. Results: A total of 141 experiments were included in the analysis. Overall mean (SD) correlation between CPP and MS was 0.56 (0.29). CPP-MS correlation strength did not correlate with baseline pressures. However, trajectory analysis revealed multiple patterns of hemodynamic and QWM evolution through untreated VF, with the most well-defined (mean coeff. = 0.58) indicating a shared bimodality temporally offset between CPP and MS. Conclusions: Hemodynamics during untreated VF show some correlation with the trajectory of QWM of the VF signal. More work is needed to understand the mechanism of this relationship.

The role of venous capacitance, circulating catecholamines, and heart rate in the hemodynamic response to increased temperature and hypoxia in the dogfish

2009 ◽  
Vol 296 (5) ◽  
pp. R1547-R1556 ◽  
Author(s):  
Erik Sandblom ◽  
Georgina K. Cox ◽  
Steve F. Perry ◽  
Anthony P. Farrell
Keyword(s):  
Heart Rate ◽  
Venous Pressure ◽  
Venous Blood ◽  
Severe Hypoxia ◽  
Venous Capacitance ◽  
Venous Circulation ◽  
Passive Flow ◽  
Increased Temperature ◽  
Blood Pressures

Hypoxia and increased temperature alter venous blood pressures in teleosts through active changes in venous tone. Elasmobranchs possess a capacious venous system but have limited adrenergic vascular innervation and subambient central venous pressure (Pcv). In this study, we explored venous hemodynamic responses to acute temperature increase and moderate (6.9 kPa) and severe (2.5 kPa) hypoxia in the dogfish ( Squalus acanthias). Normoxic dogfish at 10°C had a Pcv between −0.08 and −0.04 kPa and a mean circulatory filling pressure (Pmcf) of ∼0.12 kPa. At 16°C, heart rate ( fH), cardiac output (Q), and Pmcf increased but Pcv and plasma epinephrine and norepinephrine levels were unchanged. In contrast, moderate and severe hypoxia increased Pcv and decreased Q and stroke volume (VS). fH decreased in severe hypoxia, whereas Pmcf was unaffected despite elevated catecholamine levels. Atropine abolished hypoxic reductions in Q, VS, and fH, but Pcv still increased. In contrast to the response in teleosts, this study on dogfish suggests that venous capacitance changes associated with warming and hypoxia are minimal and likely not mediated by circulating catecholamines. Thus hemodynamic status of the capacious elasmobranch venous circulation is potentially regulated by blood volume shifts from passive flow-mediated events and possibly through myogenic mechanisms.

scholarly journals THE ROLE OF INVASIVE AND NON-INVASIVE MEASUREMENTS OF HVPG IN DECISION MAKING IN PATIENTS WITH PORTAL HYPERTENSION AND ESOPHAGEAL VARICES

2021 ◽  
Vol 74 (2) ◽  
pp. 321-326
Author(s):  
Adam Kern ◽  
Tomasz Arłukowicz ◽  
Krystian Bojko ◽  
Leszek Gromadziński ◽  
Jacek Bil
Keyword(s):  
Portal Hypertension ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Diameter Ratio ◽  
Resonance Imaging ◽  
Liver Disorders ◽  
Non Invasive ◽  
Favorable Safety ◽  
Invasive Techniques

Many researchers and clinicians have taken the value of hepatic venous pressure gradient (HVPG) as an essential prognostic factor in subjects with chronic liver disorders. And HVPG alterations characterize a predictive value in subjects at the beginning of the disease (HVPG 6 – 10 mmHg) as well as in subjects in whom hemodynamically significant portal hypertension has developed (HVPG ≥ 10 mmHg). Our review aims to present the feasibility and applicability of HVPG in modern clinical practice in patients with liver cirrhosis, including invasive and non-invasive methods. HVPG measurement is a feasible method with a favorable safety profile. However, hemodynamically significant portal hypertension also might be determined using non-invasive options as elastography, magnetic resonance imaging, and indices derived from laboratory parameters, e.g., aspartate aminotransferase-to-platelet ratio, platelet count/spleen diameter ratio, or VITRO score. Hepatic vein catheterization with the evaluation of HVPG is the current gold standard for determining portal pressure; however, new non-invasive techniques are nowadays more frequently used.

scholarly journals Mechanisms of Takotsubo cardiomyopathy; role of microcirculatory dysfunction

2016 ◽  
Vol 5 ◽  
Author(s):  
Nauman Khalid
Keyword(s):  
Takotsubo Cardiomyopathy ◽  
Imaging Techniques ◽  
Nuclear Imaging ◽  
Microvascular Dysfunction ◽  
Left Ventricular ◽  
Coronary Perfusion ◽  
Timi Frame Count ◽  
Microcirculatory Dysfunction ◽  
Reversible Left Ventricular Dysfunction

<p>Takotsubo cardiomyopathy is characterized by reversible left ventricular dysfunction typically preceded by an emotional or a physical stressor. The underlying pathophysiologic mechanisms include multivessel coronary vascular spasm, microvascular dysfunction, neurogenic stunning of the myocardium and catecholamine surge. Microcirculatory dysfunction may play a key role in the evolution of this syndrome especially in the acute phases of the illness. Severe invasive and noninvasive modalities are utilized to ascertain any compromise in coronary perfusion in Takotsubo cardiomyopathy, including Doppler guidewire technique, Thrombolysis in myocardial infarction (TIMI) frame count (TFC), TIMI myocardial perfusion grade (TMPG) and nuclear imaging techniques. TIMI frame count can be utilized as a diagnostic marker and clinical indicator in assessment of microvascular function or coronary flow in patients with Takotsubo cardiomyopathy.</p>

scholarly journals The Role of IL-6 and ET-1 in the Diagnosis of Coronary MicroVascular Disease in Women

2021 ◽  
Vol 11 (10) ◽  
pp. 965
Author(s):  
Diana Gurzău ◽  
Adela Sitar-Tăut ◽  
Bogdan Caloian ◽  
Gabriel Guşetu ◽  
Horaţiu Comşa ◽  
...  
Keyword(s):  
Left Ventricular Systolic Dysfunction ◽  
Systolic Dysfunction ◽  
Microvascular Disease ◽  
Macrovascular Disease ◽  
Microvascular Dysfunction ◽  
Left Ventricular ◽  
Functional Class ◽  
Microvascular Angina ◽  
Coronary Lesions

Background: Microvascular angina is a common clinical entity, with about a three-fold higher frequency in women. The pathogenesis of microvascular angina has not been much studied, but inflammation and endothelial dysfunction have been incriminated as the main mechanisms of this disease. Methoss: Our purpose was to analyze whether certain inflammatory markers, i.e., interleukin 6 (IL-6) and endothelin 1 (ET-1), can play a role in the diagnosis of microvascular angina in women. Results: Ninety women with ischemic heart disease were divided into two groups, based on their affliction with either microvascular or macrovascular disease. In general, the levels of IL6 and ET1 were similar between the two groups. Analyzing these marker levels according to the number of coronary lesions, we obtained an increased IL6 value that was similar for patients with microvascular angina, one-vessel, and two-vessel coronary disease, but significantly lower than in women with three-vessel coronary lesions. Also, in microvascular angina, IL6 level was correlated with the NYHA IV functional class. Unexpectedly, the level of ET1 was correlated with left ventricular systolic dysfunction. Conclusions: In women with an increased suspicion of microvascular angina, in whom microvascular dysfunction cannot be tested invasively, IL-6 level, unlike the ET-1 level, might be considered a diagnostic marker of this disease.

Microvascular (dys)Function in Stable Coronary Artery Disease: Cross Talk with Epicardial Segments

2018 ◽  
Vol 24 (25) ◽  
pp. 2900-2905
Author(s):  
Lucian Calmac ◽  
Vlad Bataila ◽  
Bogdan Dragoescu ◽  
Cosmin Mihai ◽  
Alexandru Scafa-Udriste ◽  
...  
Keyword(s):  
Coronary Flow ◽  
Stable Coronary Artery Disease ◽  
Microvascular Dysfunction ◽  
Complex Interaction ◽  
Diagnostic Tools ◽  
Pathological State ◽  
Hemodynamic Parameters ◽  
Artery Disease ◽  
Epicardial Stenosis ◽  
Current Guidelines

Myocardial ischemia is the consequence of an unbalance between coronary flow that can be achieved and myocardial metabolic needs. Pathological state of both epicardial and intramyocardial vessels may be responsible for inducing ischemia. However, revascularization decision should be based on the severity of each epicardial lesion that is evaluated. There are different diagnostic tools that may help for the evaluation of each compartment which is based on the measurement of coronary hemodynamics. Pressure-derived indices are recommended by current guidelines for evaluation of epicardial stenosis significance. We assess the complex interaction between hemodynamic parameters in order to understand how different parameters are influenced in the settings of microvascular dysfunction.

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