Additive prognostic value of high baseline coronary flow velocity to ejection fraction during resting echocardiography: 3-year prospective study.

BACKGROUND: There is a lack of information about the prognostic value of high velocity in coronary arteries during echocardiography. The present study was aimed at investigating the three-year prognostic value of coronary velocity assessment in all patients who were referred for echocardiography examination. METHODS: The prospective study comprises 747 consecutive patients. Death, myocardial infarction (MI), acute coronary syndrome (ACS), and/or revascularisation were defined as major adverse cardiac events (MACE). Routine echocardiography was added with coronary velocity assessment in the left main, anterior descending, or circumflex coronary arteries by the Doppler method. RESULTS: During a median follow-up of 36 months, 192 patients experienced MACE. Deaths occurred more frequently in patients with high local velocity in proximal left-sided segments vs. in middle left-sided segments vs. patients without high coronary velocity (9 vs. 3 vs. 1%, p < 0.0001). Death/MI/ACS occurred in 17 vs. 7 vs. 1%, p < 0.0001, respectively. Age (HR 1.04, 95% CI 1.00; 1.06; p < 0.04), a velocity more than 65 cm/s in any proximal segments of the arteries (HR 4.7, 95% CI 1.9; 11.9; p < 0.002), ejection fraction (HR 0.97, 95% CI 0.94; 0.99; p < 0.007) were strong independent prognostic predictors of death/MI/ACS. The maximal velocity of coronary flow velocity had a significant additive prognostic value to ejection fraction. CONCLUSIONS: The coronary velocity parameters give long-term prognostic information that can be used to identify persons with a high risk of MACE in consecutive non-selected patients.

New Porcine Model of Arteriovenous Fistula Documents Increased Coronary Blood Flow at the Cost of Brain Perfusion.

Background: Arteriovenous fistulas (AVF) represent a low resistant circuit. It is known that their opening leads to decreased systemic vascular resistance, increased cardiac output and other hemodynamic changes. Possible competition of AVF and perfusion of other organs has been observed before, however the specific impact of AVF has not been elucidated yet. Previous animal models studied long-term changes associated with a surgically created high flow AVF. The aim of this study was to create a simple AVF model for the analysis of acute hemodynamic changes. Methods: Domestic female pigs weighing 62.6 ± 5.2 kg were used. All the experiments were held under general anesthesia. The AVF was created using high-diameter ECMO cannulas inserted into femoral artery and vein. Continuous hemodynamic monitoring was performed throughout the protocol. Near-infrared spectroscopy sensors, flow probes and flow wires were inserted to study brain and heart perfusion. Results: AVF blood flow was 2.1 ± 0.5 L/min, which represented around 23% of cardiac output. We observed increase in cardiac output (from 7.02 ± 2.35 L/min to 9.19 ± 2.99 L/min, p = 0.0001) driven dominantly by increased heart rate, increased pulmonary artery pressure, and associated right ventricular work. Coronary artery flow velocity rose. On the contrary, carotid artery flow and brain and muscle tissue oxygenation measured by NIRS decreased significantly. Conclusions: Our new non-surgical AVF model is reproducible and demonstrated an acute decrease of brain and muscle perfusion.

The evaluation of constant coronary artery flow versus constant coronary perfusion pressure during normothermic ex situ heart perfusion.

BACKGROUND: Evidence suggests that hearts that are perfused under ex-situ conditions lose normal coronary vasomotor tone and experience contractile failure over a few hours. We aimed to evaluate the effect of different coronary perfusion strategies during ex situ heart perfusion on cardiac function and coronary vascular tone. METHODS: Porcine hearts (n = 6 each group) were perfused in working mode for 6 hours with either constant aortic diastolic pressure (40 mmHg) or constant coronary flow rate (500 mL/min). Functional and metabolic parameters, cytokine profiles, cardiac and vascular injury, coronary artery function and oxidative stress were compared between groups. RESULTS: Constant coronary flow perfusion demonstrated better functional preservation and less edema formation (Cardiac index: flow control = 8.33 vs pressure control = 6.46 mL·min-1·g-1, p = 0.016; edema formation: 7.92% vs 19.80%, p < 0.0001). Pro-inflammatory cytokines, platelet activation as well as endothelial activation were lower in the flow control group. Similarly, less cardiac and endothelial injury was observed in the constant coronary flow group. Evaluation of coronary artery function showed there was loss of coronary autoregulation in both groups. Oxidative stress was induced in the coronary arteries and was relatively lower in the flow control group. CONCLUSIONS: A strategy of controlled coronary flow during ex situ heart perfusion provides superior functional preservation and less edema formation, together with less myocardial damage, leukocyte, platelet, endothelial activation, and oxidative stress. There was loss of coronary autoregulation and decrease of coronary vascular resistance during ESHP irrespective of coronary flow control strategy. Inflammation and oxidative stress state in the coronary vasculature may play a role.

The Underlying Cardiovascular Mechanisms of Resuscitation and Injury of REBOA and Partial REBOA.

Introduction: Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) is used for aortic control in hemorrhagic shock despite little quantification of its mechanism of resuscitation or cardiac injury. The goal of this study was to use pressure-volume (PV) loop analysis and direct coronary blood flow measurements to describe the physiologic changes associated with the clinical use of REBOA. Methods: Swine underwent surgical and vascular access to measure left ventricular PV loops and left coronary flow in hemorrhagic shock and subsequent placement of occlusive REBOA, partial REBOA, and no REBOA. PV loop characteristics and coronary flow are compared graphically with PV loops and coronary waveforms, and quantitatively with measures of the end systolic and end pressure volume relationship, and coronary flow parameters, with accounting for multiple comparisons. Results: Hemorrhagic shock was induced in five male swine (mean 53.6 ± 3.6 kg) as demonstrated by reduction of stroke work (baseline: 3.1 vs. shock: 1.2 L*mmHg, p < 0.01) and end systolic pressure (ESP; 109.8 vs. 59.6 mmHg, p < 0.01). ESP increased with full REBOA (178.4 mmHg; p < 0.01), but only moderately with partial REBOA (103.0 mmHg, p < 0.01 compared to shock). End systolic elastance was augmented from baseline to shock (1.01 vs. 0.39 ml/mmHg, p < 0.01) as well as shock compared to REBOA (4.50 ml/mmHg, p < 0.01) and partial REBOA (3.22 ml/mmHg, p = 0.01). Percent time in antegrade coronary flow decreased in shock (94%-71.8%, p < 0.01) but was rescued with REBOA. Peak flow increased with REBOA (271 vs. shock: 93 ml/min, p < 0.01) as did total flow (peak: 2136, baseline: 424 ml/min, p < 0.01). REBOA did not augment the end diastolic pressure volume relationship. Conclusion: REBOA increases afterload to facilitate resuscitation, but the penalty is supraphysiologic coronary flows and imposed increase in LV contractility to maintain cardiac output. Partial REBOA balances the increased afterload with improved aortic system compliance to prevent injury.

Class of hemorrhagic shock is associated with progressive diastolic coronary flow reversal and diminished left ventricular function.

Introduction: The relationship between coronary artery flow and left ventricular (LV) function during hemorrhagic shock remains unknown. The aim of this study was to quantify coronary artery flow directionality alongside left ventricular function through the four classes of hemorrhage shock. Methods: Following baseline data collection, swine were exsanguinated into cardiac arrest via the femoral artery using a logarithmic bleed, taking each animal through the four classes of hemorrhagic shock based on percent bleed (class I: 15%; class II: 15%-30%; class III: 30%-40%; class IV: >40%). Telemetry data, left ventricular pressure-volume loops, and left anterior descending artery flow tracings over numerous cardiac cycles were collected and analyzed for each animal throughout. Results: Five male swine (mean 72 ± 12 kg) were successfully exsanguinated into cardiac arrest. Mean left ventricular end-diastolic volume, end-diastolic pressure, and stroke work decreased as the hemorrhagic shock class progressed (p < 0.001). The proportion of diastole spent with retrograde coronary flow was also associated with class of hemorrhagic shock (mean 5.6% of diastole in baseline, to 63.9% of diastole in class IV; p < 0.0001), worsening at each class from baseline through class IV. Preload recruitable stroke work (PRSW) decreased significantly in classes II through IV (p < 0.001). Systemic Vascular Resistance (SVR) is associated with class of hemorrhage shock (p < 0.001). Conclusion: With progressive classes of hemorrhagic shock left ventricular function progressively decreased, and the coronary arteries spent a greater proportion of diastole in retrograde flow, with progressively more negative total coronary flow. Preload recruitable stroke work, a load-independent measure of inotropy, also worsened in severe hemorrhagic shock, indicating the mechanism extends beyond the drop in preload and afterload alone.

Cerebral blood flow alteration following acute myocardial infarction in mice.

Heart failure is associated with low cardiac output (CO) and low brain perfusion that imposes a significant risk for accelerated brain ageing and Alzheimer's disease (AD) development. Although clinical heart failure can emerge several years following acute myocardial infarction (AMI), the impact of AMI on cerebral blood flow (CBF) at early stages and up to 30 days following MI is unknown. Sixteen months old male mice underwent left anterior descending (LAD) coronary artery ligation. Hemodynamics analyses were performed at baseline and at days 1, 7, and 30 post-MI. Left ventricular (LV) ejection fraction (EF), LV volumes, CO, and right common carotid artery (RCCA) diameter were recorded by echocardiography. RCCA flow (RCCA FL) was measured by Doppler echocardiography. LV volumes consistently increased (P<0.0012) and LV systolic function progressively deteriorated (P<0.0001) post-MI. CO and RCCA FL showed a moderate but significant decrease over the course of MI with similar fluctuation pattern such that both variables were decreased at day 1, increased at day 7, and decreased at 30 days post-MI. Correlation and regression analyses between CO and RCCA FL showed a strong correlation with significance at baseline and day 30 post-MI (R = 0.71, P=0.03, and R = 0.72, P=0.03, respectively). Days 1 and 7 analyses between CO and RCCA FL showed moderate correlation with non-significance post-MI (R = 0.51, P=0.2, and R = 0.56, P=0.12, respectively). In summary, CBF significantly decreased following AMI and remained significantly decreased for up to 30 days, suggesting a potential risk for brain damage that could contribute to cognitive dysfunction later in life.

Role of Coronary Flow Velocity in Predicting Adverse Outcome in Clinical Practice.

There is a lack of information on the prognostic value of local high velocity in coronary arteries during echocardiography. The aim of the study described here was to define the prognostic value of local velocity >70 cm/s in the left main, anterior or circumflex artery during echocardiography. There were 412 patients in the prospective study. Death, non-fatal myocardial infarction, acute pulmonary edema, acute coronary syndrome and revascularization were defined as major adverse cardiac events (MACEs). Over 10.5 mo, there were 207 patients with MACEs. Seventeen patients died, 10 had non-fatal acute cardiac events and 184 underwent revascularization. Deaths occurred in patients with high local velocity (6.4% vs. 0%, p <0.009). Acute cardiac events occurred in 10% versus 0% (p <0.003). MACEs were observed in 62% versus 0% (p <0.0000001). Only maximal velocity was an independent prognostic predictor of death (odds ratio = 1.02, 95% confidence interval: 1.01-1.03, p <0.02) and MACEs (odds ratio = 1.04, 95% confidence interval: 1.02-1.05, p <0.0001). The success rate of coronary artery visualization for at least one segment was 91%.

Platelet counts on admission affect coronary flow, myocardial perfusion and left ventricular systolic function after primary percutaneous coronary intervention.

BACKGROUND: Patients with acute ST-elevation myocardial infarction (STEMI) and increased platelet count treated by fibrinolysis have worse outcomes. AIM: The aim of this study was to test the hypothesis that platelet blood count at admission in patients with acute STEMI treated by primary percutaneous coronary intervention affects coronary flow, myocardial perfusion and recovery of left ventricular systolic function. METHODS: A total of 174 patients presenting with acute anterior STEMI and treated with primary percutaneous coronary intervention were included and divided into subgroups of admission platelet blood count of <200 K, 200-300 K, 300-400 K and >400 K. Evaluation of coronary artery flow and myocardial blush grade was performed according to the TIMI criteria. Electrocardiographic ST elevation resolution post-primary percutaneous coronary intervention was evaluated. Doppler echocardiographic evaluation of left anterior descending coronary artery velocities early and late after primary percutaneous coronary intervention and assessment of left ventricular ejection fraction and wall motion score index (WMSI) of left ventricular and left anterior descending coronary artery territory were performed. RESULTS: Post-primary percutaneous coronary intervention TIMI, myocardial blush grade and ST elevation resolution were similar in all groups. Patients with platelet counts <200 K had higher peak diastolic left anterior descending coronary artery velocity both early and late after primary percutaneous coronary intervention, and higher prevalence of left anterior descending coronary artery velocity deceleration time exceeding 600 ms, (45.5% vs. 40%, P<0.05). Patients with platelet counts >400 K presented with worse left ventricular ejection fraction, left ventricular WMSI and left anterior descending coronary artery WMSI, and before discharge this subgroup had worse left ventricular WMSI and left anterior descending coronary artery WMSI, P<0.01. CONCLUSIONS: Patients with anterior STEMI treated by primary percutaneous coronary intervention with lower admission platelet count had higher left anterior descending coronary artery diastolic velocities, better myocardial perfusion with more patients having left anterior descending coronary artery-descending coronary artery velocity deceleration time >600 ms. Patients with higher platelet counts had lower left ventricular systolic function both at admission and before discharge.

Left anterior descending coronary artery flow after primary angioplasty in acute anterior ST-elevation myocardial infarction: how much flow is needed for left ventricular functional recovery?

UNLABELLED: The treatment of choice in acute ST-elevation myocardial infarction (STEMI) is primary percutaneous coronary intervention (PPCI). Although, thrombolysis in myocardial infarction (TIMI) and myocardial blush grade (MBG) measures provide semi-quantitative flow evaluation after PPCI, serial and quantitative volumetric flow evaluation is still lacking. AIM: Serial assessment of left anterior descending (LAD) coronary artery flow in patients with anterior myocardial infarction (MI), immediately after PPCI, 48 h later and pre-discharge and compare findings in patients with optimal and suboptimal PPCI result and their relation to left ventricular ejection fraction (LVEF). METHODS: Velocities in the LAD were recorded within 6 h after PPCI and one week later in 36 patients presenting with acute anterior STEMI. Sixteen patients had TIMI and MBG less than 3 after PPCI were considered to have suboptimal result. Sampling of LAD coronary artery velocity was obtained from trans-thoracic Doppler. Flow in the LAD coronary artery was estimated using heart rates, Doppler time velocity integrals and LAD color Doppler diameters. RESULTS: Diastolic LAD coronary artery flow immediately after PPCI in subjects with suboptimal PPCI, 29 ± 21 ml/min was lower than in those with optimal result, 39.8 ± 21 ml/min, p<0.05. Diastolic flow in the LAD coronary artery increased to 50.3 ± 28.5 ml/min two days after PPCI in patients with suboptimal PPCI, p=0.04, and to 49.6 ± 13.8 ml/min in those optimal result, p=0.04. LVEF increased by 9% in patients with optimal PPCI, p=0.004, and did not change in the other group. CONCLUSIONS: (a) After PPCI, flow in the LAD coronary artery was dynamic; (b) in the presence of suboptimal PPCI, early LAD coronary artery flow was reduced; (c) pre-discharge, LAD coronary artery flow increased; and (d) LVEF increased only in optimal PPCI group associated with higher early LAD coronary artery flow.

Ultrasound bio-microscopy for measurement of coronary artery flow and estimation of infarct size in a mouse model of acute myocardial infarction.

Ultrasound bio-microscopy was used to measure hemodynamic changes in the left main coronary artery after myocardial infarction (MI), and its usefulness in estimating infarct size was evaluated. MI was induced by left anterior descending artery ligation. Diastolic peak velocity (Vd), mean flow velocity (Vmean) and the velocity-time integral (VTI) were measured 2 and 6 h after MI. Serum troponin I levels were assayed 2, 6 and 12 h after MI. At 2 h, Vmean and VTI significantly differed between mice that underwent low and high left anterior descending artery ligation; Vd, Vmean and VTI were correlated with infarct size (r = -0.557, -0.693 and -0.672, respectively; all p < 0.01). Infarct size was more strongly correlated with 2-h ultrasound bio-microscopy measurements than with 2-h serum troponin I level. Measurement of coronary artery blood flow by ultrasound bio-microscopy may be useful for early estimation of infarct size in mice.

A patient came back with retrograde coronary flow in the distal right coronary artery 2 years after coronary intervention: clinical significance of retrograde coronary flow to detect coronary artery occlusion.

A 69-year-old male patient, who had a history of coronary stent implantation to the proximal right coronary artery (RCA), presented with exertional chest pain. Transthoracic Doppler echocardiography revealed retrograde coronary flow in the distal RCA, and treadmill stress echocardiography revealed inducible myocardial ischemia in the inferior and posterior segments. Coronary angiography demonstrated a severe stenotic lesion with flow delay in the mid RCA and collateral circulation to the distal RCA from the left coronary artery. Detection of retrograde coronary flow in the distal RCA using transthoracic Doppler echocardiography is a useful method to diagnose subtotal occlusion of the RCA.