Determinants Of Myocardial Oxygen Consumption Research Articles

A pathophysiological compass to personalize antianginal drug treatment.

Myocardial ischaemia results from coronary macrovascular or microvascular dysfunction compromising the supply of oxygen and nutrients to the myocardium. The underlying pathophysiological processes are manifold and encompass atherosclerosis of epicardial coronary arteries, vasospasm of large or small vessels and microvascular dysfunction - the clinical relevance of which is increasingly being appreciated. Myocardial ischaemia can have a broad spectrum of clinical manifestations, together denoted as chronic coronary syndromes. The most common antianginal medications relieve symptoms by eliciting coronary vasodilatation and modulating the determinants of myocardial oxygen consumption, that is, heart rate, myocardial wall stress and ventricular contractility. In addition, cardiac substrate metabolism can be altered to alleviate ischaemia by modulating the efficiency of myocardial oxygen use. Although a universal agreement exists on the prognostic importance of lifestyle interventions and event prevention with aspirin and statin therapy, the optimal antianginal treatment for patients with chronic coronary syndromes is less well defined. The 2019 guidelines of the ESC recommend a personalized approach, in which antianginal medications are tailored towards an individual patient's comorbidities and haemodynamic profile. Although no antianginal medication improves survival, their efficacy for reducing symptoms profoundly depends on the underlying mechanism of the angina. In this Review, we provide clinicians with a rationale for when to use which compound or combination of drugs on the basis of the pathophysiology of the angina and the mode of action of antianginal medications.

A study on rate pressure product in south Indian pregnant women with anaemia

Background: Anaemia is a cause of serious concern and contributes to a significantly higher maternal mortality. Rate Pressure Product (RPP) is a major determinant of myocardial oxygen consumption and blood flow. There is an increase in oxygen demand in anemia. Thus, in the present study, we have compared the difference in RPP between a normal pregnant women and pregnant women with anemia.Methods: A total of 180 pregnant women (normal pregnant woman - 90 and pregnant woman with anaemia - 90) belonging to different trimesters of pregnancy were included in the study. Age, height, and weight were recorded, and their body mass index was calculated. The systolic blood pressure, diastolic blood pressure, heart rate was recorded and RPP was calculated.Results: There was a significant increase in RPP in pregnant woman with anaemia in all three trimesters of pregnancy, but the significant increase was more in the third trimester.Conclusions: The present study shows that there is an increase in RPP in pregnant woman with anaemia and they are more prone to hemodynamic stress and cardiovascular risks, especially in their third trimester of pregnancy. This hemodynamic change may be taken into account to prevent the cardiovascular complications associated with anemia in pregnancy. Thus, RPP can be used as a sensitive non-invasive simple marker for early diagnosis of cardiovascular disease in pregnant woman.

Limitation of Infarct Size and the Open Artery Hypothesis: A Conversation With Eugene Braunwald, MD.

Eugene Braunwald received an MD from the New York University School of Medicine. He completed an internal medicine residency at Johns Hopkins Hospital and cardiology fellowships at Mount Sinai Hospital, Columbia University, and the National Heart Institute. He served as chief of cardiology and subsequently clinical director of the institute. From 1968 to 1972, he was the founding chair of medicine at the University of California, San Diego. From 1972 to 1996, he served as chair of medicine at the Brigham and Women’s Hospital. In 1975, he was elected to the National Academy of Sciences. He is now the Distinguished Hersey Professor of Medicine at Harvard Medical School and a senior investigator of the TIMI Study Group, which he founded in 1984. Dr Braunwald replies: I became aware of the importance of AMI in 1951 during an elective in cardiology during my senior year at the New York University School of Medicine. At the time, AMI was by far the most common cause of death in adults in the United States. Of the patients who survived to be admitted to hospitals (no one knew how many AMI patients failed to reach hospital emergency departments), about one third died before discharge, either suddenly, presumably from an arrhythmia, or secondary to pump failure. Of the patients who were discharged alive, about one quarter died within a year, most frequently as a consequence of heart failure or recurrent MI. Pathologists had taught that AMI was usually associated with coronary thrombosis. Indeed, during my cardiology elective, Herrick’s classic article describing AMI was required reading. Its title, “Clinical Features of Sudden Obstruction of the Coronary Arteries,” showed how these 2 conditions (coronary occlusion and AMI) were intertwined.1 My direct involvement in the care of several patients who did not survive the acute event left …

Effect Of Verapamil On a Speed Of The Excitation Wave Conduction In The Isolated Rat Heart Myocardium

Effect Of Verapamil On a Speed Of The Excitation Wave Conduction In The Isolated Rat Heart Myocardium

Effect of esmolol infusion on myocardial oxygen consumption during extubation and quality of recovery in elderly patients undergoing general anesthesia: randomized, double blinded, clinical trial

BackgroundUpon recovery from anesthesia and during extubation, there will be mechanical stimulation of receptors in the respiratory tract that results in both respiratory and cardiovascular reflex responses. Heart rate plays a major determinant of myocardial oxygen consumption and cardiac workload, so decreasing the heart rate will increase the ischemic threshold and improve the cardiac performance.ObjectiveTo evaluate the effect of esmolol infusion on myocardial oxygen consumption during extubation and quality of recovery in elderly patients undergoing general anesthesia.MethodsHundred adult patients ASA I & II scheduled for elective open unilateral inguinal hernia were randomized, double-blindly into one of two parallel groups, esmolol group (E) (n = 50) and control group (C) (n = 50). In the esmolol group, 1 mg/kg esmolol was given as bolus over 30 s then followed by a continuous esmolol infusion of 100 μg/kg/min starting 10 min before end of surgery till 5 min after extubation. While patients in group C received normal saline bolus of the same volume followed by a continuous normal saline infusion of the same volume per hour as group E. Mean heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), mean blood pressure (MBP), rate pressure product (RPP), anesthesia time, recovery time, postoperative nausea & vomiting, number of doses of antiemetic agent and quality of extubation were recorded.ResultsThe results showed that patients in the esmolol group had lower values of (RPP) after esmolol infusion with statistically significant difference when compared with patients in the control group using unpaired t-test (P < 0.05), this will decrease oxygen consumption in esmolol group. Also, there was statistically significant difference between both groups regarding values of HR (beat/min), SBP (mmHg), DBP (mmHg) and MBP (mmHg) starting 2 min after esmolol infusion and continued till 10 min after extubation using unpaired t-test (p < 0.05). As regards PONV, there was lower incidence in esmolol group when compared to control group using unpaired t-test with statistically significant difference (P < 0.05).ConclusionsEsmolol is a safe, effective and well-tolerated drug that can be used in elderly patients undergoing general anesthesia to reduce the myocardial oxygen consumption and improve the quality of recovery.

The significance of rate pressure product in heart failure patients

&lt;p&gt;&lt;span&gt;Introduction: &lt;/span&gt;The rate pressure product (RPP) is a strong determinant of myocardial oxygen consumption, and relates strongly to important indices for morbidity and cardiovascular mortality. Its significance in Black-African subjects with heart failure (HF) has however not been well described. This study therefore aimed to assess the significance of RPP among admitted HF patients in 2 Nigerian centres.&lt;/p&gt;&lt;p&gt;&lt;span&gt;Methods: &lt;/span&gt;Admitted HF patients in the 2 centres were serially recruited after satisfying all inclusion criteria. RPP was calculated by multiplying heart rate by systolic blood pressure at admission. Subjects were classified into 2 groups based on RPP &amp;lt;10,000 (log10 &amp;lt;4.0) (group 1) or above (group 2), which is a cut-off value above which there is increased risk of myocardial ischemia.&lt;/p&gt;&lt;p&gt;&lt;span&gt;Results: &lt;/span&gt;100 subjects were recruited from the 2 centres with a mean age of 47.3+/-19.5 years, and 53% were females. 35% of the subjects were in group 1 while 65% were in group 2. N-Terminal B-type Natriuretic Peptide (NTBNP), serially measured in only 37 subjects (12 in group 1; 25 in group 2), was significantly higher in group 1 as compared with group 2 (p=0.016). Group 1 also had lower interventricular septal thickness(IVST) (p=0.007) as compared with group 2 subjects. RPP correlated strongly with IVST (r=+0.510, p&amp;lt;0.001), left ventricular posterior wall thickness (LVPWT) (r=+0.399, p&amp;lt;0.001) and LV end-diastolic dimension (LVEDD) (r=-0.202, p=0.045). Log10 &amp;gt;4.0 was strongly associated with IVST (95%confidence interval (CI): 1.061-1.528, p=0.009) and NT-BNP (CI:0.999-1.000, p=0.026). There was however no significant relationship (p&amp;gt;0.05) between RPP and in-hospital mortality, severity of dyspnoea, gender, age, body weight, LV ejection fraction or presence of atrial fibrillation/flutter.&lt;/p&gt;&lt;p&gt;&lt;span&gt;Conclusion: &lt;/span&gt;This study confirms the close relationship that exists between a determinant of myocardial oxygen consumption (RPP), and indices for LV wall tension (IVST, LVEDD and NT-BNP), in Black-Africans with HF.&lt;/p&gt;

The Regional Myocardial Flow–Function Relationship

This pioneering article was the first to quantitatively relate regional myocardial blood flow (microspheres) to regional contractile function (sonomicrometry). Regional flow and function were more or less proportionately reduced during acute ischemia in conscious dogs. The notion that myocardial ischemia arises from an imbalance between oxygen demand and supply goes originally back to the characterization of hemodynamic determinants of myocardial oxygen consumption in the whole heart and the observation that decreases or increases, respectively, in heart rate or ventricular function decrease or increase, respectively, the severity of ischemic injury.1 However, myocardial ischemia is in most instances a regional event. It was not until into the 1970s that experimental techniques became available to measure myocardial blood flow and contractile function on a regional level, notably the microsphere technique2 and sonomicrometry.3 Stephen Vatner in his classic article4 was the first to use both techniques simultaneously and quantitatively relate subendocardial segment shortening to subendocardial blood flow. He characterized the flow–function relationship as exponential during acute coronary stenosis in conscious dogs, with a more steep and almost linear part at more severe stenosis. Admittedly, the measurements were restricted to only the subendocardial layer, and segment …

Myocardial Protection by Volatile Anesthetics in Patients Undergoing Cardiac Surgery: A Critical Review of the Laboratory and Clinical Evidence

JOHN BLAND AND EDWARD LOWENSTEIN first reported in 1976 that administration of halothane (0.75 minimum alveolar concentration [MAC]) significantly (p o 0.001) attenuates ST-segment elevation caused by brief coronary artery occlusion in 6 dogs anesthetized with chloraloseurethane concomitant with a reduction in the primary determinants of myocardial oxygen consumption. These experiments demonstrated, for the first time, that volatile anesthetics are capable of producing essential anti-ischemic effects. Since the publication of this landmark paper, several studies provided further evidence that volatile anesthetics protected myocardium against reversible and irreversible ischemic injury. For example, isoflurane and halothane enhanced the functional recovery of postischemic-reperfused (‘‘stunned’’) canine myocardium when either volatile anesthetic was administered before a 15-min coronary artery occlusion and reperfusion. This beneficial effect occurred in conjunction with the preservation of high-energy phosphates. Isoflurane also reduced the magnitude of myocardial necrosis and improved recovery of left ventricular (LV) function after global ischemia and reperfusion. Halothane was shown to maintain contractile function and ultrastructural integrity during reperfusion after normothermic cardioplegic arrest in isolated rat hearts. These results were especially notable because they implied that the protective action of volatile anesthetics occur independent of any favorable alteration in coronary perfusion or myocardial oxygen supply-demand relations. In 1997, three research groups simultaneously reported that the administration of halothane or isoflurane before prolonged coronary artery occlusion and reperfusion reduced myocardial infarct size in vivo. This beneficial effect was termed ‘‘anesthetic preconditioning’’ (APC), occurred independent of changes in systemic and coronary hemodynamics, and persisted despite discontinuation of the volatile anesthetic before coronary artery occlusion, a ‘‘memory’’ period similar to that observed during ischemic preconditioning (IPC). Subsequently, volatile anesthetics were shown to protect myocardium against ischemic

Work-related sickness absence negotiations: GPs' qualitative perspectives

GPs can find their role as issuers of sickness certification problematic, particularly in trying to maintain a balance between certifying absence and preserving the doctor-patient relationship. Little research has been published on consultations in which sickness absence has been certified. To explore negotiations between GPs and patients in sickness absence certification, including how occupational health training may affect this process. A qualitative study was undertaken with GPs trained in occupational health who also participate in a UK wide surveillance scheme studying work-related ill-health. Telephone interviews were conducted with 31 GPs who had reported cases with associated sickness absence. Work-related sickness absence and patients' requests for a 'sick note' vary by diagnosis. Some GPs felt their role as patient advocate was of utmost importance, and issue certificates on a patient's request, whereas others offer more resistance through a greater understanding of issues surrounding work and health acquired through occupational health training. GPs felt that their training helped them to challenge beliefs about absence from work being beneficial to patients experiencing ill-health; they felt better equipped to consider patients' fitness for work, and issued fewer certificates as a result of this. Complex issues surround GPs' role in the sickness-certification process, particularly when determining the patient's ability to work while maintaining a healthy doctor-patient relationship. This study demonstrates the potential impact of occupational health training for GPs, particularly in light of changes to the medical statement introduced in 2010.

Eugene Braunwald

In the last issue of Circulation Research ,1 we heard from esteemed cardiologist Eugene Braunwald (Harvard Medical School and Brigham and Women’s Hospital, Boston, MA) about his family’s escape from Nazi-occupied Austria. Braunwald arrived in the United States with his family in 1939, aged 10. He went on to become one of the most influential and highly regarded clinical cardiovascular scientists of the last 50 years. It is safe to say that through his research, Braunwald has contributed to the survival of countless heart attack patients across the globe. In part two of this interview, we learn how Braunwald’s passion for cardiology developed and how at 80 years of age that passion, as well as his work ethic, show no signs of diminishing. ### So, a New Life in Brooklyn Began… Thankfully, we were out of danger, but my parents were now concerned about our future as strangers in a country that, contrary to current belief, was not yet out of the depression. We were as poor as the proverbial church mice, and my father had to figure out how to support us. I don’t know how, but he always managed to put bread on the table. Life was nothing like it had been in Vienna before March 1938. But, my father was a very enterprising, strongly motivated, and hard-working man, and after a few false starts, he managed, with my mother’s help, to create a second successful wholesale clothing business. ### Tell Me About Your School Days in Brooklyn I started in an elementary school and did well. In fact, I was the class Valedictorian, which was quite an honor for a relatively recent arrival. Then, I went off to Brooklyn Technical High School, an elite public high school that required passing a very tough entrance examination. ### You Were Already Leaning Toward the Sciences. At What Point Did You Decide to Study Medicine? I started high school with the desire to become an engineer. It was the “in thing” to do …

Impaired coronary artery vasodilation during skin surface cooling in healthy older adults

Cardiovascular‐related mortality increases in the cold winter months, particularly in older adults. To determine whether coronary artery blood flow responses to skin surface cooling differ with age, we studied 9 young (25±1 yrs) and 10 older healthy adults (65±2 yrs). We hypothesized that left anterior descending coronary artery blood velocity (CBV) responses, measured using Doppler transthoracic echocardiography, to skin surface cooling (15–18° C water perfused suit for 20 min) would be impaired with age. We found that cooling increased left ventricular wall stress, a determinant of myocardial oxygen consumption, in young (185.6±6.5 to 202.9 ±10.4 mmHg, P &lt; 0.05) and older adults (189.1±8.8 vs. 222.7±14.7 mmHg, P &lt; 0.01) although the magnitude of this response was twofold greater in older adults (Δ9.13±3.48% vs. Δ17.62±3.24%, young and older, respectively; P=0.09). Despite increased left ventricular wall stress during cooling in young and older adults CBV increased only in the young (20.86±1.32 to 25.56±1.24 cm/s, p&lt;0.01) and not older group (17.60±1.09 to 19.93 ±0.97 cm/s, p=0.11). These data suggest that an impaired coronary vasodilator response to cold stress may contribute to age‐dependent increases in cardiovascular‐related mortality during the winter months in healthy adults.Support: NIH HL92309, AG24420 and M01 RR10732

Elevated Heart Rate in Cardiovascular Diseases: A Target for Treatment?

Heart rate is a major determinant of myocardial oxygen consumption and of cardiac work, and thus reduction of heart rate may represent an important strategy for the treatment of patients with a wide range of cardiac disorders. In addition, several experimental lines of research point to high heart rate as an important risk factor for atherosclerosis and, thus, pharmacologic heart rate reduction could prevent or retard the development of atherosclerotic plaques and increase survival. Today, in patients with acute or chronic coronary syndromes or with congestive heart failure, reducing heart rate is a generally accepted treatment modality. Up to now, no human study has been performed to demonstrate the efficacy and the risk-benefit ratio of cardiac slowing in patients without cardiac disorders. However, recent retrospective analyses of the INternational VErapamil-SR/trandolapril STudy and the Paris Prospective Study 1 provided promising results. Treatment of high heart rate in healthy subjects appears to be premature, but in clinical conditions such as hypertension or diabetes, the reduction of elevated heart rate appears a desirable additional goal of therapy.

BEAUTIFUL: ivabradine for reducing coronary artery disease

hasbrought heart rate once again intofocus as a potential cardiovascularrisk factor . It is clear that the hear t-rate reduction due to beta-blockerspartially accounts for the improvedprognosis in patients with heartfailure and left ventricular (LV)dysfunction complicating coronaryartery disease. In addition heartrate is a key determinant ofmyocardial oxygen consumption,and chronotropic therapy is asso-ciated with improvement ofischaemic symptoms. However,beta-blockers are not universallyprescribed or tolerated at full dosesin these patients because of side-effects and contraindications.

Pathophysiological role of heart rate: from ischaemia to left ventricular dysfunction

Myocardial ischaemia results from imbalance between myocardial oxygen demand and supply. An increase in heart rate (HR) will raise both demand and supply. HR is the most important determinant of myocardial oxygen consumption and of cardiac energy demand. HR reduction improves myocardial perfusion by increasing the fraction of the cardiac cycle occupied by diastole, which accounts for 80% of coronary flow. Besides these physiological characteristics, HR is also linked to the progression of atherosclerosis, at least in animals, and an increase in HR is associated with plaque rupture in humans. The symptom of chest pain in stable angina is almost always triggered by elevated HR owing to physical or emotional stress. Equally, an increased HR precedes an episode of asymptomatic or silent myocardial ischaemia. Therefore, it is not surprising that the efficacy of some anti-anginal drugs such as b-blockers and non-dihydropyridine calcium antagonists has been related to their effectiveness in reducing HR. In many studies, multivariate analysis has shown HR to be an independent predictor of mortality and of hospitalization for heart failure. A relationship has been found between HR reduction and mortality in patients with congestive heart failure treated with b-blockers. Thus HR is an important therapeutic target for ischaemia and left ventricular dysfunction or congestive heart failure, and it seems likely that relatively high HR is both causative and indicative of important pathophysiological processes: HR is a risk factor for cardiovascular morbidity and mortality throughout the cardiovascular continuum.

Thyroid hormone is an independent determinant of myocardial oxygen consumption in patients with heart failure

Thyroid hormone is an independent determinant of myocardial oxygen consumption in patients with heart failure

Overview of large morbidity/mortality trials with ivabradine: focus on the BEAUTIfUL study

Heart failure and left ventricular dysfunction complicating coronary artery disease (CAD) are associated with a poor prognosis. Beta-blockers have been shown to be beneficial for survival in these conditions, a benefit that is mediated, in part, through slowing of the heart rate. In addition, since heart rate is one of the major determinants of myocardial oxygen consumption, its lowering is associated with relief of ischaemia and anginal symptoms, and indeed, slowing the heart rate with betablockers is associated with effective relief of ischaemia. Therefore, in left ventricular dysfunction complicating CAD, there is potentially a major role for slowing the heart rate. Although effective, beta-blockers may not always achieve optimal heart rate lowering or may not be well tolerated. Ivabradine, a selective heart rate-lowering agent, is being tested compared with placebo, in addition to standard therapy (including beta-blockers, if tolerated) in the large morbidity/mortality BEAUTIfUL trial. This study was established to test the superiority of ivabradine compared with placebo as an adjunct to conventional therapy in the reduction of a composite endpoint of cardiovascular mortality, acute myocardial infarction (requiring hospital admission), and new or worsening heart failure (requiring hospital admission) in patients with stable CAD, in sinus rhythm, and with left ventricular dysfunction. Approximately 11 000 patients with evidence of CAD, a sinus rhythm of � 60 bpm, and an ejection fraction of 39% or less were enrolled. In a randomized, double-blind fashion, patients are receiving ivabradine 5 mg twice daily titrated to 7.5 mg twice daily after 2 weeks, or matching placebo, in order to target a heart rate of ,60 bpm. Holter electrocardiography, echocardiography, and NT-proBNP substudies are also planned. The BEAUTIfUL trial will be an important step in determining the clinical importance of heart rate on the outcome of patients with CAD and left ventricular dysfunction.

Future perspectives of If inhibition in various cardiac conditions

Heart rate (HR) is a major determinant of myocardial oxygen consumption and myocardial perfusion in patients with ischaemic heart disease. Large epidemiological studies have demonstrated that high resting HR is a strong predictor of total and cardiovascular mortality in the healthy population and in patients with hypertension, in patients with metabolic syndromes, in the elderly, and in patients with coronary artery disease (CAD). HR modulation with beta-blockers has shown favourable effects on post-myocardial infarction mortality in correlation with their HR-lowering actions. In this regard, because of their pharmacological action, inhibitors of the sinus pacemaker I f current, agents that exclusively reduce HR, may be of particular importance as antianginal agents, and have potential utility in reducing morbidity and mortality in cardiovascular disorders in patients with CAD and in patients with heart failure. Sinus tachyarrhythmias are a heterogeneous group of disorders that are often difficult to manage. A pure HR reduction may be a novel way of treatment for these patients.

Editorial: heart rate

In 1997, Levine1 reviewed the theory of the relationship between heart rate and life span. From observations in the animal kingdom, smaller animals have higher heart rates and shorter life spans than do large animals. This is simply explained by a biophysical imperative in which the ratio of heat loss, which is a function of body mass, increases as body size decreases. Calculations also show that the number of heart beats per lifetime is unexpectedly constant among mammals, despite a 40-fold difference in life span. The difference in body weight is even greater, of the order of 500,000-fold, from hamster to whale. Azbel2 stressed the concept and suggested that life expectancy is predetermined by the basic energetics of living cells, and the inverse relationship between longevity and heart rate reflects an epiphenomenon in which heart rate is a marker or a determinant of metabolic rate and energetic requirements. This linear inverse relationship between heart rate and life expectancy is valid for all mammals except humans. Humans have a mean heart rate of 70 beats/min and a life expectancy of 80 years.1 The reason why the relationship does not apply to humans may reside in advances in science, medicine and technology. The observation that lowering heart rate just from 70 to 60 beats/min would increase life expectancy from 80 to 93.3 years in humans is surprising. In contrast, in the general population it has been observed that the risk for death from all causes, including cardiovascular diseases, increases with resting heart rate. Several clinical studies have shown that increased heart rate is an important risk factor for cardiovascular morbidity and mortality, not only in patients with established heart disease3 and cardiovascular risk factors such as hypertension,4 but also in the general population.5 Heart rate is a major determinant of myocardial oxygen consumption and metabolic demand, and consequently of cardiac workload. A reduction in heart rate would therefore elevate the ischaemic threshold and improve cardiac performance. Several drugs are used in the treatment of cardiovascular diseases but only two classes at present can reduce the heart rate, namely the beta-blockers and some of the calcium channel blockers. It is interesting that reduction in heart rate by beta-blockers has two favourable consequences: first, a decrease in blood pressure, with consequent reduced myocardial oxygen requirements; and, second, a longer diastolic filling time associated with a slower heart rate, allowing for increased coronary perfusion. Betablockers have been consistently shown to reduce cardiovascular mortality, sudden death and reinfarction in patients recovering from acute myocardial infarction.6—8 The primary actions of beta-blockers are to reduce both resting heart rate and the response of heart rate to exercise. The magnitude of mortality reduction, non-fatal reinfarction and infarct size with beta-blockers is clinically meaningful. Diltiazem and verapamil, among the calcium channel blockers, lower heart rate by 6—7 beats/min and have both been shown to decrease the risk for death and non-fatal reinfarction in survivors of acute myocardial infarction with no clinical heart failure or impaired left ventricular function.9,10 Correspondence: Prof. Roberto Ferrari, Cattedra di Cardiologia, University of Ferrara and Fondazione S. Maugeri, IRCCS, Cardiovascular Pathophysiology Research Centre, Corso Giovecca, 203, 44100 Ferrara, Italy.

Association of left ventricular hypertrophy regression and heart rate reduction with determinants of myocardial oxygen consumption and cardiovascular events: The LIFE study

Association of left ventricular hypertrophy regression and heart rate reduction with determinants of myocardial oxygen consumption and cardiovascular events: The LIFE study

High thoracic epidural anesthesia in coronary surgery

High thoracic epidural anesthesia and analgesia are being increasingly used for coronary artery bypass graft surgery. The reasons for this include excellent perioperative pain control with advantage of early tracheal extubation, improved postoperative pulmonary function, and cardiac protection due to sympthatetic blockade. Cardiac protection is the consequence of decreased heart rate, myocardial contractility and arterial blood pressure, without changes in coronary perfusion pressure. Therefore, high thoracic epidural analgesia beneficially alters major determinants of myocardial oxygen consumption, without jeopardizing coronary perfusion pressure. In addition, decrease of functional residual capacity, may reduce postoperative pulmonary morbidity. Patients with high thoracic epidural anesthesia revealed a more favourable perioperative hemodynamic profile, lower incidence of ischemia and better response to perioperative stress. The epidural catheter should be placed at the Th2/Th3 interspace at least one hour before administration of heparin. After local anesthetic bolus dose, a continuous epidural infusion is recommended. There is strong evidence for beneficial effects of high thoracic epidural anesthesia in patients undergoing surgical myocardial revascularization. However, it is still underutilized in current clinical practice.