Prevention Of Myocardial Ischemia Research Articles

Vitamin D deficiency and electrocardiographic subclinical myocardial injury: Results from National Health and Nutrition Examination Survey‐III

Association of cardiovascular disease (CVD) with nontraditional risk factors such as vitamin D deficiency has been examined previously. An investigation of the association of vitamin D with subclinical myocardial injury (SC-MI) based on an electrocardiographic score is a simple, cost-effective and innovative way to explore this relationship. We hypothesize that low vitamin D levels will be associated with prevalent SC-MI independent of traditional CVD risk factors, lifestyle factors, and socioeconomic status. This analysis included 6079 participants (58.3 ± 13.1 years; 54.1% women) without CVD from the third National Health and Nutrition Examination Survey. A multivariable logistic regression model was used to examine the association between vitamin D categories (<20, 20-29, and >30 ng/mL (reference) and cardiac injury score. There was an incremental increase in the prevalence of SC-MI across vitamin D categories with the highest prevalence in <20 ng/mL, followed by 20 to 29 ng/mL and then >30 ng/mL (trend P-value <0.0001). There was a statistically significant association between vitamin D deficiency (<20 ng/mL) and SC-MI (odds ratio [OR] (95% confidence interval [CI]): 1.27 (1.04-1.55), P = 0.04). This association was stronger in men than women (OR (95% CI): 1.74 (1.32-2.30) vs 0.94 (0.70-1.25) respectively; interaction P-value 0.002). Vitamin D deficiency is associated with SC-MI, especially in men. These findings may further highlight the role of nontraditional risk factors in the development of CVD. The value of vitamin D supplementation in the prevention of myocardial ischemia and injury may warrant investigation.

Integration of Metabolomics With Pharmacodynamics to Elucidate the Anti-myocardial Ischemia Effects of Combination of Notoginseng Total Saponins and Safflower Total Flavonoids.

Notoginseng (Sanqi), the roots and rhizomes of Panax notoginseng and safflower, the flowers of Carthamus tinctorius, are widely used traditional Chinese medicines (TCMs) for the treatment of cardiovascular diseases. Positive evidences have fueled growing acceptance for cardioprotective effects of the combination of the notoginseng total saponins and safflower total flavonoids (CNS) against myocardial ischemia (MI). However, the underlying cardioprotective mechanisms of CNS are still obscured. Metabolomics is a comprehensive tool for investigating biological mechanisms of disease, monitoring therapeutic outcomes, and advancing drug discovery and development. Herein, we investigated the cardioprotective effects of CNS on the isoproterenol (ISO)-induced MI rats by using plasma and urine metabolomics based on ultra-performance liquid chromatography coupled with quadrupole-time of flight mass spectrometry (UPLC-Q-TOF/MS) and multiple pharmacodynamics approaches. The results showed that pretreatment with CNS could attenuate the cardiac injury resulting from ISO, as evidenced by decreasing the myocardial infarct size, converting the echocardiographic, histopathological, and plasma biochemical abnormalities, and reversing the perturbations of plasma and urine metabolic profiles, particularly for the 55.0 mg/kg dosage group. In addition, 44 metabolites were identified as the potential MI biomarkers, mainly including a range of free fatty acids (FFAs), sphingolipids, and glycerophospholipids. CNS pretreatment group may robustly ameliorate these potential MI-related biomarkers. The accumulation of LysoPCs and FFAs, caused by PLA2, may activate NF-κB pathway and increase proinflammatory cytokines. However, our results showed that CNS at 55.0 mg/kg dosage could maximally attenuate the NF-κB signaling pathway, depress the expressions of TNF-α, IL-6, IL-1β, and PLA2. The results suggested that the anti-inflammatory property of CNS may contribute to its cardioprotection against MI. Our results demonstrate that the integrating of metabolomics with pharmacodynamics provides a reasonable approach for understanding the therapeutic effects of TCMs and CNS provide a potential candidate for prevention and treatment of MI.

Ginsenoside Rg1 protects cardiomyocytes from hypoxia-induced injury through the PI3K/AKT/mTOR pathway.

Myocardial ischemia (MI) is a leading cause of morbidity and mortality which makes the prevention and control of MI tremendously important. We aimed to explore the functional roles of ginsenoside (Gin) Rg1 in cardiomyocytes under hypoxia and to clarify underlying mechanisms. Hypoxia-induced H9c2 cell injury was evaluated by alterations of cell viability, apoptosis and autophagy. Then, effects of Gin Rg1 on hypoxia-induced cell injury were measured. The activation of the phosphatidylinositol-3-kinase (PI3K)/AKT/mechanistic target of rapamycin (mTOR) pathways as well as expression of hypoxia-inducible factor 1α (HIF-1α) was determined with or without addition of PI3K or mTOR inhibitor. Finally, the effects of Gin Rg1 on rat ischemia/reperfusion (I/R) injury and underlying mechanism were studied. First of all, hypoxia was identified to induce a decrease in cell viability and to increase cell apoptosis and autophagy. Then, these hypoxia-induced alterations were ameliorated by Gin Rg1, which had no effect on cell viability under normoxia. Subsequently, the phosphorylated levels of key kinases in the PI3K/AKT/mTOR pathways as well as expression of HIF-1α were all elevated by Gin Rg1. Activation of the PI3K/AKT/mTOR pathways and HIF-1α expression were inhibited by PI3K inhibitor, and activation of mTOR pathway and HIF-1α expression were inhibited by mTOR inhibitor. More in vivo experiments proved that Gin Rg1 ameliorated rat I/R injury through activating the PI3K/AKT/mTOR pathways. Gin Rg1 protected cardiomyocytes from hypoxia-induced cell injury by upregulating HIF-1α through activation of the PI3K/AKT/mTOR pathways.

Management of Diastolic Heart Failure

The diastolic heart failure also referred to as heart failure with preserved left ventricular systolic function (preserved ejection fraction). The difference between systolic and diastolic HFs is a pathophysiological one and isolated forms of left ventricular dysfunction are rarely observed. In diastolic HF left ventricular systolic function is normal or only slightly impaired, and the typical manifestations of HF result from increased filling pressure caused by impaired relaxation and compliance of the left ventricle. The management should include antihypertensive treatment, maintenanceof the sinus rhythm, prevention of tachycardia, venous pressure reduction, prevention of myocardial ischemia and prevention of diabetes mellitus. Treatment of diastolic HF is aimed to stop the progression of the disease, relieve its symptoms, eliminate exacerbations and reduce the mortality. The predisposing factors for diastolic dysfunction include elderly age, female sex, obesity, coronary artery disease, hypertension and diabetes mellitus. The European Society of Cardiology specifies the type of therapy in diastolic HF based on: angiotensin converting enzyme inhibitors, angiotensin receptor blockers, beta-blockers, non dihydropyridine calcium channel blockers, diuretics.

Treatment of hypertension in heart failure with preserved ejection fraction.

Prevalence of Heart Failure with Preserved Ejection (HFPEF) has been rising steadily in the recent past. Studies have shown that at least half of patients presenting with symptoms and signs of heart failure (HF) have preserved left ventricular ejection fraction, i.e. HFPEF, and that this portion of the HF population consists predominantly of women, older age group, and people with hypertension and other cardiovascular risk factors. The morbidity and mortality associated with HFPEF are much higher than the normal population. Chronic hypertension is the most common cause in addition to age, with suggestion of up to 60% of patients with HFPEF being hypertensive. Addressing the specific aetiology and aggressive risk factor modification remain the mainstay in the treatment of HFPEF. Current guidelines recommend the management should involve treatment of hypertension, control of heart rate, venous pressure reduction, and prevention of myocardial ischemia. This review aims to discuss the role of hypertension in the pathophysiology, risk stratification and prognosis of HFPEF, as well as the current available data on various antihypertensive options in this population.

Anesthetic management for severe aortic regurgitation in an infant repaired by Ross procedure

We report the anesthetic management of a 7-month-old male infant with severe aortic regurgitation (AR) scheduled for the Ross procedure. To the best of our knowledge, this is the first report from the viewpoint of anesthetic management for the Ross procedure performed in an infant. He had been suffering from severe AR that occurred suddenly when he was 5 months old. The cause of the AR was considered to be spontaneous rupture of a fenestrated aortic valve, owing to congenital tissue defect in part of the aortic valvular leaflet. The Ross procedure was scheduled to be performed under general anesthesia using deep hypothermic cardiopulmonary bypass (CPB). Continuous infusion of nitroglycerin was started during CPB and continued after CPB to dilate the newly implanted coronary arteries for the prevention of myocardial ischemia and to decrease afterload and pulmonary vascular resistance. Weaning from CPB was performed without difficulty, but after the prolonged CPB he had a bleeding tendency that needed transfusion and a hemostatic drug. Monitoring with transesophageal echocardiography was very useful for evaluating myocardial ischemia, and for assessing the procedure and the completion of surgical repair. His postoperative course was uneventful and he was discharged on the 25th postoperative day.

Comparison of active and passive coronary perfusion in off-pump coronary artery bypass grafting

The myocardial protective effects of active and passive coronary perfusion were compared during off-pump coronary artery bypass grafting (OPCAB) in coronary stenosis model. An internal shunt tube was placed in the proximal left anterior descending arteries of adult dogs to produce a 75% coronary stenosis model. In 10 animals passive coronary perfusion was performed using an internal shunt tube placed in a pseudo-anastomotic site, and active coronary perfusion was performed through an external shunt tube. Ischemia was examined at normal and low blood pressure, based on hemodynamics, regional myocardial blood flow, and oxygen and lactate extraction in the perfused area. With passive perfusion, regional myocardial blood flow decreased and oxygen extraction and regional lactate production increased at normal blood pressure, indicating myocardial ischemia. Regional myocardial blood flow further decreased at low blood pressure. In contrast, regional myocardial blood flow with active perfusion did not change at normal or low blood pressure, and oxygen and lactate extraction were unchanged, indicating prevention of myocardial ischemia. Myocardial ischemia can occur with passive perfusion even at normal blood pressure. Active coronary perfusion that provides sufficient regional perfusion prevents myocardial ischemia during coronary artery anastomosis in OPCAB.

Pre-Emptive Conditioning of the Ischemic Heart

Ischemic heart disease remains one of the most frequent causes of morbidity and mortality worldwide. Although the prognosis of myocardial ischemia has been dramatically improved by the techniques of early reperfusion, the prevention of irreversible ischemic damage remains a critical aspect of the treatment. An appealing novel therapeutic avenue for the prevention of myocardial ischemia relates to the possibility of a pre-emptive conditioning of the heart, in which an activation of survival pathways could be achieved in patients with ischemic heart disease who are at risk for a subsequent lethal ischemia. These patients would include those with unstable angina, or with severe and repetitive ischemic episodes, and patients scheduled for surgical revascularization. In these situations, the pre-emptive activation of survival signaling mechanisms would confer a prophylactic cardioprotection during the following ischemic stress. During the last twenty years, it became clear that the heart can trigger survival mechanisms when submitted to stress, in such conditions as myocardial stunning, hibernation and preconditioning. The goal of the pre-emptive conditioning is to activate such survival pathways as a prophylactic measure to prevent myocardial cell death when the heart is threatened by potentially lethal ischemia. Based on the experimental data collected at the bench side, we review how this approach could be applied in the clinical setting.

Clinical role and efficacy of landiolol in the intensive care unit

Beta-adrenergic receptor blockers have proved to be effective for the management of various cardiovascular diseases and the prevention of perioperative cardiac events and cerebrovascular accidents. Landiolol is a short-acting beta-blocker, with high beta 1-selectivity and a short duration of action. We thought landiolol was valuable and suitable for intensive care unit (ICU) patients, and conducted a retrospective study. The records of 80 patients (58 post-surgical patients; group S and 22 internal medicine patients; group IM) were reviewed. Thirty-seven (64%) of the group S patients were post-coronary artery bypass graft surgery, and the IM group consisted mostly of patients with acute myocardial infarction. The most common indication for landiolol in group S was the prevention of myocardial ischemia (50%), and in group IM, it was atrial fibrillation (45%). The median infusion rate of landiolol was 5 microg.kg(-1).min(-1) and the median infusion time was 2 days. Twenty-six patients were continued on oral beta-adrenergic receptor blockers. Landiolol reduced heart rate significantly without reducing blood pressure, and stabilized hemodynamics. We confirmed that landiolol is valuable as a bridge to starting oral beta-adrenergic receptor blockers and as an anti-arrhythmic agent, and that it is suitable for ICU patients due to its high beta 1-selectivity and rapid onset and offset of action.

Intravenous glucose–insulin–potassium during off‐pump coronary artery bypass surgery does not reduce myocardial injury

This randomized, double-blind, placebo-controlled study was designed to determine whether an intra-operative, intravenous infusion of glucose-insulin-potassium (GIK) could be helpful in the prevention of myocardial ischemia and in the maintenance of intra-operative cardiac performance in patients undergoing off-pump coronary artery bypass (OP-CAB) surgery. Eighty two adults undergoing elective OP-CAB surgery were randomly divided into two groups that received intravenously either 5% dextrose in water or GIK (50% dextrose in 500 ml of water; regular insulin, 125 IU; potassium, 80 mmol) at 0.75 ml/kg/h immediately before the induction of anesthesia to the end of surgery. To evaluate myocardial damage, creatine kinase MB and troponin T were measured before surgery, immediately after arrival in the intensive care unit and on the first post-operative day. To assess cardiac performance, hemodynamic data were obtained before and after the induction of anesthesia, before and after the bypass graft and after sternal closure. Blood glucose was measured at the same time. There was no significant difference in cardiac enzymes, hemodynamic parameters and blood glucose between the two groups. The use of vasoactive, inotropic and/or anti-arrhythmic agents, insulin and supplemental glucose was not significantly different between the groups. The results suggest that the intravenous administration of GIK during OP-CAB surgery neither reduces myocardial damage nor improves intra-operative cardiac performance in patients without contractile dysfunction.

Inhibition of Rho-Kinase by Hydroxyfasudil Prevents Vasopressin-Induced Myocardial Ischemia in Donryu Rats by Attenuating Coronary Vasoconstriction

Background: Inhibition of rho-kinase has been shown to attenuate vasopressin (AVP)-induced myocardial ischemia measured as S-wave depression in Donryu rats. This has been attributed to a direct inhibitory effect on AVP-induced coronary vasoconstriction. However, since AVP also increased mean arterial blood pressure (MAP) which was attenuated by the rho-kinase inhibitors used, the prevention of myocardial ischemia could have been due to effects on afterload. Results: The purpose of this study was to determine if rho-kinase inhibition prevents S-wave depression independent of the effects on blood pressure. In anesthetized Donryu rats (200–340 g), infusion of AVP (0.1 IU/kg) resulted in a sustained increase in MAP (ΔMAP = 46 ± 7 mm Hg) and a transient S-wave depression (–90 ± 20 µV). Infusion of phenylephrine titrated to achieve a comparable pressor response (ΔMAP = 52 ± 2 mm Hg) resulted in a significantly smaller S-wave depression (–30 ± 20 µV). Pretreatment with the rho-kinase inhibitor, hydroxyfasudil (3 mg/kg), decreased MAP by –28 ± 2 mm Hg and significantly attenuated AVP-induced S-wave depression (–10 ± 10 µV) compared to AVP. When rats were pretreated with phenylephrine titrated to maintain MAP, hydroxyfasudil still significantly attenuated AVP-induced S-wave depression (–14 ± 12 µV). Hydralazine (1 mg/kg), which lowered MAP by –36 ± 5 mm Hg, had no significant effect on AVP-induced S-wave depression (–105 ± 32 µV). Conclusion:These data indicate that inhibition of rho-kinase with hydroxyfasudil attenuates AVP-induced myocardial ischemia independent of changes in MAP and are consistent with an inhibitory effect on coronary vasoconstriction.

Heart Rate Reduction: A Potential Target for the Treatment of Myocardial Ischaemia

Because most of myocardial perfusion takes place during diastole, reducing the heart rate is likely to have anti-ischaemic effects. The present paper reviews the role of heart rate in relation to coronary artery disease outcome, as well as ways to reduce heart rate in the clinical setting. Nonpharmacological intervention, and particularly exercise training, has a definite effect on both heart rate reduction and the prevention of myocardial ischaemia. The protective role of β-blockers after acute myocardial infarction is amply documented; their anti-ischaemic efficacy appears to be attributable to their effect on heart rate, but also to their role in cardiac inotropism. Recently, the If (funny) current inhibitor ivabradine, which has a potent heart rate reduction effect without any haemodynamic effect has demonstrated anti-ischaemic efficacy in a randomised trial versus placebo, as well as in trials where it showed an effect similar to that of the conventional anti-ischaemic agents amlodipine and atenolol. In addition, such an agent, which does not influence myocardial contractility, might be particularly valuable in the setting of myocardial stunning or acute left ventricular failure at the acute stage of myocardial infarction. However, only future studies will determine whether isolated heart rate reduction will have the same protective efficacy as that of β-blocking agents in secondary prevention after myocardial infarction.

Trimetazidine Limits the Effects of Myocardial Ischaemia During Percutaneous Coronary Angioplasty

SummaryThis open-label, randomised, controlled study is aimed at assessing the effect of pre-treatment with the metabolic agent trimetazidine on the degree of ischaemia during percutaneous transluminal coronary angioplasty (PTCA).Overall 44 patients with one-vessel coronary artery stenosis (>70%) in the medial part of the left anterior descending artery were included. One group (n = 22) was pre-treated with oral trimetazidine. The other group (n = 22) was the control. All patients (n = 44) were administered aspirin and conventional treatment.All patients underwent PTCA; stents were implanted in 11 trimetazidine patients and in seven control patients.The mean ST-segment elevation during all balloon inflations was significantly lower in the trimetazidine group than in the control group (−1.66 ± 1.50 mm vs. 3.29 ± 1.59 mm, p = 0.001). Maximal ST-segment elevations andmean ST elevation values during sequential balloon inflations were also significantly lower with trimetazidine (p = 0.018). The mean amplitude of the T-wave alterations during all balloon inflations was significantly lower with trimetazidine (3.09 ± 2.39 mm vs. 6.83 ± 4.31 mm; p = 0.001). Similarly, the maximal amplitude of the T-wave alterations was 4.50 ± 2.90 mm with trimetazidine vs. 9.25 ± 4.97 mm in control patients (p = 0.0005). Angina and rhythm disturbances were more frequent in the control group. Time from balloon inflation to onset of angina was 50 ± 26.2s with trimetazidine vs. 32 ± 15.0s, for control group (p = 0.03). The time to pain relief after deflation was 19.3 ± 11.4s with trimetazidine vs. 28.2 ± 16.8s (p = 0.001).Trimetazidine administered a few days before PTCA appears to be a cardioprotective agent for the prevention of myocardial ischaemia.

Anaesthesia for abdominal aortic surgery

Anaesthesia for the abdominal aortic surgery patient may be considered a major professional challenge owing to patient- as well as surgery-associated risk factors. The aortic patient is characterized by generalized atherosclerotic disease evidenced by high prevalence of hypertension, heart disease, cerebrovascular disease and impaired renal function. Diabetes and chronic obstructive lung disease may further complicate the preoperative state of health and influence the perioperative course. General anaesthesia, in elective cases often in combination with epidural analgesia, is commonly used. Important issues of the anaesthetic management are adequate monitoring of vital organ function and therapeutic measures (fluids, pharmacological support) for the maintenance of haemodynamic stability and prevention of myocardial ischaemia, splanchnic hypoperfusion, spinal cord ischaemia and renal failure. The aortic cross-clamping and declamping procedures are associated with acute cardiovascular stress influencing the haemodynamic stability. At the release of the clamp, measures should also be taken to minimize the risk of reperfusion type of cellular injury occurring. Furthermore, measures for intraoperative heat preservation are essential for prevention of hypothermia-induced adverse metabolic and cardiovascular events in the postoperative period. The outcome of the patient with ruptured abdominal aortic aneurysm is dependent on the resuscitation skills and anaesthetic management of the anaesthesiologist and the surgical experience and skill of the vascular surgeon.

Beta Blockade in Non-cardiac Surgical Patients

Beta Blockade in Non-cardiac Surgical Patients

The effects of transmural pressure on prostacyclin release from porcine endocardial endothelial cells--comparison with vascular endothelial cells.

We assessed the effect of pressure on the release of prostacyclin (PGI2) from cultured endocardial endothelial cells (EECs) and vascular endothelial cells (VECs). EECs were harvested from the right ventricle (RV) and left ventricle (LV) of porcine hearts, and VECs from pulmonary artery (PA), aorta (Ao) and coronary artery (CA). Confluent EECs and VECs were incubated for 30 min under various pressures (0, 50, 100, 150 mmHg) and PGI2 release from each cell was measured. Pressure-induced PGI2 release from LV-EECs was larger than that from RV-EECs. Pressure also increased PGI2 release from both PA- and Ao-VECs, but not from CA-VECs. These findings suggest that endocardium can produce PGI2 in response to pressure and PGI2 released into the coronary blood from the ventricle may play an important role in the prevention of myocardial ischemia.

Minimising cardiac anaesthetic risk: the tortoise or the hare?

There is no doubt that a group of patients at increased risk of peri-operative cardiac morbidity exists and must be managed with the emphasis on the prevention of myocardial ischaemia. It is also clear that a potentially far larger group are at risk of failing to meet the increased cardiovascular and metabolic demands of surgery and therefore suffering the consequences of a relative hypoperfusion injury. Pre-operative assessment must address both groups and management regimens sought to provide optimal outcome for both. At present there is no consistent strategy for their identification, assessment or management of the high risk surgical population despite the fact that they probably consume a disproportionate share of hospital resources. The first and most important step is the recognition that this high risk group exists. Only then can this population be given similar consideration to those currently thought to be at risk of ischaemia.

The patient with coronary artery disease scheduled for noncardiac surgery

Summary Cardiovascular morbidity continues to represent the single most important contributor to surgical mortality. The impact of postoperative interventions in potentially improving cardiovascular morbidity and mortality is extremely difficult to separate from the influence of the intra-operative technique. It is most likely that the combination of techniques used intra-operatively and postoperatively have a combined impact on cardiovascular outcome. A thorough preoperative assessment of the patient to determine the probability of risk for coronary artery disease and whether further workup will improve patient outcome is essential. Perioperative interventions such as coronary artery bypass grafting have not always shown a subsequent reduction in patient morbidity before noncardiac surgery. Other perioperative interventions such as percutaneous transluminal coronary angioplasty and the insertion of an intraaortic balloon pump may provide more patient benefit with less risk than coronary artery bypass graft. Intra-operative monitoring devices are only helpful if clinicians can interpret and extrapolate meaningful data that will assist them in achieving an end-point (detection and prevention of myocardial ischemia) for their patient's management. A familiarity of the sensitivity and specificity of a particular monitoring device is helpful to determine the best method for detecting myocardial ischemia. A smooth transition from the intraoperative to the postoperative period is desirable. Attenuation of the neurohumeral stress response through adequate pain management may reduce the incidence of postoperative morbid cardiac events. Regional techniques may hold the greatest promise for effecting significant improvements in cardiovascular outcome. Yeager's study is conclusive in showing that epidural anesthesia and analgesia results in decreased morbidity and mortality for major vascular surgery patients. Tuman 55 showed decreased hypercoagulability with epidural anesthesia that may be a critical physiological benefit in reducing the incidence of vascular graft occlusion, coronary artery occlusion, and deep venous thromboses. Blomberg's studies in patients with severe coronary artery disease provide insight into the mechanisms by which epidural anesthesia may be a therapeutic measure in preventing and treating myocardial ischemia. Perhaps we should consider using thoracic epidural anesthesia for patients with coronary artery disease scheduled for noncardiac surgery to reduce the incidence or even the occurrence of perioperative myocardial infarction. Perhaps thoracic epidural anesthesia will replace our conventional therapies for myocardial ischemia. Only further investigation of this hypothesis will elucidate the answer.

Zur Prophylaxe myokardialer Isch�mien Untersuchung w�hrend aortokoronarer Bypassoperation mit dem Kalziumantagonisten Diltiazem*

The incidence of postoperative myocardial infarction (MI) is proportional to the incidence of myocardial ischaemic episodes. Therefore, the prevention of such episodes is of great clinical importance. METHODS. In 90 patients undergoing coronary artery bypass grafting (CABG), perioperative i.v. treatment with either nitroglycerin (NTG), diltiazem (DIL), or the combination of DIL/NTG was used until arrival in the intensive care unit. Myocardial ischaemic episodes were monitored with an automatic ECG-ST-trend analyser (Marquette 7010). RESULTS. Significantly less ischaemic episodes were seen in the DIL group (6.7%) compared to the NTG group (13.2%) or DIL/NTG group (13.5%). Furthermore, significantly less ischaemic episodes were associated with relevant haemodynamic alterations in the DIL group (58.1%) compared to the NTG (89.1%) or DIL/NTG group (80.0%). Increases in heart rate were markedly reduced in the DIL group. DISCUSSION. DIL results in marked haemodynamic stabilisation during CABG, especially in the period immediately after extra-corporeal circulation. This might serve as an explanation for the significant reduction in ischaemic episodes in the DIL group compared to the other two groups. Therefore, perioperative prevention of myocardial ischaemia with the calcium antagonist DIL seems to be favourable in patients during CABG.

The effect of coronary bypass graft surgery for the prevention of sudden cardiac death: recurrent episodes after ICD implantation and review of literature.

Sudden cardiac death (SCD) accounts for at least 50% of the mortality of patients with ischemic heart failure. Ventricular arrhythmias are responsible for most cases of sudden cardiac death. There is some evidence that coronary artery bypass graft (CABG) surgery may reduce the incidence of recurrent episodes of SCD by prevention of myocardial ischemia. To test the hypothesis that CABG surgery is effective in the prevention of SCD, we compared the recordings of implantable cardioverter defibrillators (ICD) in patients who underwent ICD implantation alone (n = 64) or ICD implantation and concomitant CABG surgery respectively (n = 11). All patients had experienced out of hospital cardiac arrest. ICD recordings were obtained every 3 months and the number of recurrent episodes of ventricular tachycardia (VT) for each time period was noted. Three months following ICD implantation patients in the surgically treated group had an average of one episode of VT per patient as compared to 2.7 episodes in the nonsurgical group. This difference was observed during the following months as well. However, at no time (up to 18 months of follow-up) this difference reached statistical significance. There were no deaths in the surgically treated group. Although we could not demonstrate a statistical significant difference between the two groups, there was a tendency in the surgically treated group to have less episodes of recurrent VT than in the medically treated group. We, therefore, conclude that survivors of SCD presenting with multivessel coronary artery disease (CAD) should undergo coronary artery bypass grafting to prevent myocardial ischemia as the triggering event for lethal ventricular arrhythmias.