Function In Coronary Heart Disease Research Articles

Potential preservative mechanisms of cardiac rehabilitation pathways on endothelial function in coronary heart disease.

Cardiac rehabilitation, a comprehensive exercise-based lifestyle and medical management, is effective in decreasing morbidity and improving life quality in patients with coronary heart disease. Endothelial function, an irreplaceable indicator in coronary heart disease progression, is measured by various methods in traditional cardiac rehabilitation pathways, including medicinal treatment, aerobic training, and smoking cessation. Nevertheless, studies on the effect of some emerging cardiac rehabilitation programs on endothelial function are limited. This article briefly reviewed the endothelium-beneficial effects of different cardiac rehabilitation pathways, including exercise training, lifestyle modification and psychological intervention in patients with coronary heart disease, and related experimental models, and summarized both uncovered and potential cellular and molecular mechanisms of the beneficial roles of various cardiac rehabilitation pathways on endothelial function. In exercise training and some lifestyle interventions, the enhanced bioavailability of nitric oxide, increased circulating endothelial progenitor cells (EPCs), and decreased oxidative stress are major contributors to preventing endothelial dysfunction in coronary heart disease. Moreover, the preservation of endothelial-dependent hyperpolarizing factors and inflammatory suppression play roles. On the one hand, to develop more endothelium-protective rehabilitation methods in coronary heart disease, adequately designed and sized randomized multicenter clinical trials should be advanced using standardized cardiac rehabilitation programs and existing assessment methods. On the other hand, additional studies using suitable experimental models are warranted to elucidate the relationship between some new interventions and endothelial protection in both macro- and microvasculature.

Effect of amiodarone hydrochloride tablets combined with potassium magnesium aspartate on hemodynamics and cardiac function in patients with coronary heart disease and arrhythmia

Purpose: To investigate the effects of amiodarone hydrochloride tablets combined with potassium magnesium aspartate on hemodynamics and cardiac function in coronary heart disease (CHD) patients with arrhythmia.Methods: In this retrospective research, a total of 110 CHD and arrhythmia patients on admission at Jiaozhou Central Hospital of Qingdao from June 2020 to June 2022 were randomly but equally divided into control group (CG) treated with propafenone hydrochloride tablets, and study group (SG) treated with a combination of amiodarone hydrochloride tablets and potassium magnesium aspartate. Clinical efficacy of the treatment types as well as the number of premature ventricular contractions (PVC), QTc interval and heart rate (HR) of the patients were monitored to determine left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), and cardiac index (CI). Fibrinogen levels, plasma viscosity and hematocrit of the patients were also assessed.Results: The total effectiveness/efficacy of treatment in SG was 92.73 %, which was significantly higher than the corresponding CG value of 76.36 % (p < 0.05). Relative to CG, PVC and HR in SG were significantly lower, while QTc interval was significantly higher. The levels of LVESD and LVEDD were significantly lower in SG than in CG, while CI level was significantly higher. However, fibrinogen, plasma viscosity and hematocrit values were significantly lower in SG than in CG (p < 0.05).Conclusion: When administered along with potassium magnesium aspartate in the treatment of CHD and arrhythmia, amiodarone hydrochloride tablets enhances clinical efficacy and improves electrocardiograph index, hemodynamics and cardiac function. Nonetheless, there is need for expanded clinical trials before the use of this treatment strategy in clinical practice.

Long-term consumption of a mediterranean diet or a low-fat diet on kidney function in coronary heart disease patients: The CORDIOPREV randomized controlled trial

Lifestyle and dietary habits influence kidney function, playing an important role in the prevention and development of chronic kidney disease (CKD). The effectiveness of the Mediterranean diet in preserving kidney function has been seen in primary prevention. However, no scientific evidence is currently available to determine which dietary pattern is more effective in the management of CKD in secondary cardiovascular disease prevention. Thus, our aim was to evaluate the efficacy of the long-term consumption of two healthy dietary patterns (a Mediterranean diet rich in extra-virgin olive oil (EVOO) compared to a low-fat diet rich in complex carbohydrates) in preserving kidney function in coronary heart disease (CHD) patients. CHD patients (n=1002) from the CORDIOPREV study were randomized to follow a Mediterranean diet (35% fat, 22% MUFA, <50% carbohydrates) or a low-fat diet (28% fat, 12% MUFA, >55% carbohydrates). Kidney function was assessed by the determination of serum creatinine-based estimated glomerular filtration rate (eGFR) at baseline and after 5-years of dietary intervention. Patients were classified according to their type 2 diabetes (T2DM) status, using baseline eGFR (normal eGFR: ≥ 90mL/min/1.73m2; mildly-impaired eGFR: 60 to <90mL/min/1.73m2, severely-impaired eGFR: <60mL/min/1.73m2) to evaluate its influence on the progression of kidney function. Multiple linear regression analysis were performed to determine the contribution of different clinical and anthropometric parameters to changes in eGFR. Although eGFR declined after both dietary interventions compared to baseline (all p<0.001), the Mediterranean diet produced a lower decline of eGFR compared to the low-fat diet in patients with T2DM (p=0.040). This effect was also observed when the overall population was considered (p=0.033). No significant differences were observed in eGFR between the two diets in non-T2DM patients. In addition, this differential effect of the Mediterranean diet was mainly observed in patients with mildly-impaired eGFR in which this diet slowed eGFR progression (p=0.002). The long-term consumption of a Mediterranean diet rich in EVOO, when compared to a low-fat diet, may preserve kidney function, as shown by a reduced decline in eGFR in CHD patients with T2DM. Patients with mildly-impaired eGFR may benefit more from the beneficial effect of the consumption of the Mediterranean diet in preserving kidney function. These findings reinforce the clinical benefits of the Mediterranean diet in the context of secondary cardiovascular disease prevention. URL, http://www.cordioprev.es/index.php/en. Clinicaltrials.gov number, NCT00924937.

The Relationship between Endothelial Nitric Oxide Synthase with Dyslipidemia in Coronary Heart Disease

BACKGROUND: Dyslipidemia is a medical condition that refers to an abnormal of blood lipids level, most common is hyperlipidemia. Elevation of blood lipid such as cholesterol, triglycerides, low-density lipoprotein (LDL) cholesterol, or a low high-density lipoprotein (HDL) cholesterol level induces disturbance of endothelial function. Endothelial dysfunction in dyslipidemia is in large part due to a reduced bioavailability of nitric oxide (NO) which is synthesized by endothelial NO synthase (eNOS) which will trigger the development of atherosclerosis, and increases the risk of coronary heart disease (CHD).&#x0D; AIM: This study aims to determine the relationship of lipid profiles of dyslipidemia with eNOS levels in CHD patients.&#x0D; MATERIALS AND METHODS: This study design was a cross-sectional study. The sample in this study was 26 patients which diagnosed as CHD of outpatients in the department of cardiology of a regional general hospital and fulfilled the inclusion and exclusion criteria. Fifteen healthy individuals who come for the general check-up were included as a control group. Blood samples were collected for measurements of eNOS levels and lipid profiles that carried out according to laboratory standards. Statistical analyses were conducted using analysis of variance and Shapiro–Wilk test.&#x0D; RESULTS: The results of this study showed that eNOS levels in the group of CHD patients (24.174 ± 7.136 ng/ml) were significantly lower (p &lt; 0.05) than those in the control group (72.092 ± 30.065 ng/ml). The mean of triglycerides and HDL levels has a weak correlation with the level of eNOS (p &gt; 0.05). The mean of LDL level has moderately positive correlation with eNOS, while cholesterol has a moderate negative correlation with the level of eNOS (p &gt; 0.05).&#x0D; CONCLUSION: This study concluded that high cholesterol levels and low HDL levels in dyslipidemia condition were correlated with eNOS, which has a protective function in CHD.

Mitral annulus displacement measured by two-dimensional speckle tracking imaging to assess the left ventricular longitudinal systolic function in coronary heart disease.

To assess the clinical utility of measuring mitral annulus displacement (MAD) by two-dimensional speckle tracking for the rapid evaluation of left ventricular longitudinal systolic function in patients with coronary heart disease (CHD). Left ventricular longitudinal systolic function was evaluated by MAD using speckle tracking echocardiography in 30 healthy volunteers (controls) as well as in 30 patients with mild, 30 patients with moderate, and 30 patients with severe CHD. All participants had their apical four-chamber and two-chamber view echocardiographic images recorded. Left ventricular end-diastolic volume, left ventricular end-systolic volume, and left ventricular ejection fraction were calculated by the biplane Simpson method. MAD of interventricular septum (MADsep), left ventricular lateral wall (MADlat), and the middle point of the mitral annulus (MADmid) were measured offline with speckle-tracking echocardiography. MADmid% was defined as MADmid divided by left ventricular end-diastolic diameter. MADmid% was 16.9 ± 1.9, 11.8 ± 3.2, 11.8 ± 2.9, and 10.3 ± 3.6, respectively, in controls and in patients with mild, moderate, and severe CHD. All MAD indexes were lower in patients with moderate or severe CHD than in controls or patients with mild CHD. MAD is an early and rapid index for the assessment of left ventricular longitudinal systolic function in patients with different degrees of coronary artery disease.

The effect of reactive oxygen species on whole blood aggregation and the endothelial cell-platelet interaction in patients with coronary heart disease

BackgroundThe effect of reactive oxygen species (ROS) on platelet function in coronary heart disease (CHD) is complex and poorly defined. Platelet aggregation studies in healthy volunteers have demonstrated contrasting results when platelets are exposed to ROS. We investigated the effect of ROS on whole blood aggregation (WBA) and the endothelial cell-platelet interaction in patients with CHD. Methods and ResultsROS generated by xanthine and xanthine oxidase caused a concentration-dependent inhibition of WBA in blood from healthy donors and patients with CHD. In patients with CHD, 100μM xanthine and 100mU/ml xanthine oxidase inhibited WBA in response to 3μg/ml collagen by 28.9% (95% CI 15.9%-41.8%, p<0.001) and in response to 5μM ADP by 36.0% (95% CI 9.6%-62.4%, p=0.005). Using nitrotyrosine expression, platelets isolated from patients with CHD were found to be susceptible to peroxynitrite damage. The addition of 1×105 cultured endothelial cells inhibited WBA in response to 3μg/ml collagen by 31.2% (95% CI 12.2%-50.2%, p<0.05) and in response to 5μM ADP by 31.6% (95% CI 2.5-60.7%, p<0.05). Addition of xanthine and xanthine oxidase did not alter this effect, however pre-treatment of endothelial cells with a nitric oxide synthase inhibitor (L-NAME) partly reversed the inhibition. ConclusionROS inhibit WBA in blood from patients with CHD. Whilst endothelial cells also inhibit WBA, the effect is attenuated by L-NAME, suggesting that nitric oxide is likely to remain an important protective mechanism against thrombosis in CHD.

Accuracy of measurement of left ventricular volume and function in coronary heart disease with real-time threedimensional echocardiography

Objective To evaluate the accuracy of measurement of left ventricular(LV) volume and function in coronary heart disease(CHD) by real-time three-dimensional echocardiography(RT-3DE) using cardiac magnetic resonance imaging (CMRI).Methods LV end diastolic volume(EDV),LV end systolic volume(ESV) and LV ejection fraction(EF) were measured with RT-3DE in patients with CHD ( n =37) and in the control ( n =30).The results measured by RT 3DE were compared with those of CMRI.The diagnostic value of RT-3DE was evaluated using receiver operating characteristic(ROC) curve.Results Compared with that measured by CMRI,EDV,ESV and EF by RT 3DE( P ＞0.05) were almost similar as that in the control.Area under ROC curve of in EDV and ESV were 0.912 and 0.944 in the control.However,EDV determined by RT-3DE was smaller than that by CMRI( P ＜0.05) in CHD group.A difference (10.95 ± 31.26 ml) was existed in EDV between the two methods.ESV measured by RT-3DE was smaller than that calculated by CMRI( P ＞0.05) with a mean differance of (3.17 ± 16.42)ml in CHD group.EF by RT-3DE( P ＞0.05)was almost as same as that by CMRI in CHD group,with a mean difference of (1.54 ± 11.85)％.The area under ROC curve of EDV and ESV were 0.834 and 0.873 in CHD group and their diagnostic performance was moderate.Conclusions Measurment of LV volume and function by RT 3DE in control was more acurrate than that in CHD.In the cases of LV remodeling in patients with CHD,RT-3DE would underestimate the LV volume. Key words: Echocardiography,real time three-dimentional; Coronary disease; Ventricular functionleft; Cardiac volume; Magnetic resonance imaging

Celecoxib activates PI-3K/Akt and mitochondrial redox signaling to enhance heme oxygenase-1-mediated anti-inflammatory activity in vascular endothelium

Although nonsteroidal anti-inflammatory drugs (NSAIDs) provide important control of pain and inflammation, they have been overshadowed by concerns regarding atherothrombotic complications. However, celecoxib seems to have a relatively good cardiovascular profile and may improve endothelial function in coronary heart disease. This led us to the hypothesis that celecoxib induces the vasculoprotective enzyme heme oxygenase-1 (HO-1). In human umbilical vein and aortic endothelial cells, 24–48 h treatment with celecoxib induced HO-1 mRNA and protein expression and increased HO-1 enzyme activity. This effect was not seen with rofecoxib or indomethacin. Supplementation of culture medium with iloprost or prostaglandin E 2 failed to reverse celecoxib-mediated HO-1 induction, indicating a cyclooxygenase-independent mechanism. Rather, this action of celecoxib involved generation of mitochondria-derived reactive oxygen species, Akt phosphorylation, and nuclear translocation of the transcription factor Nrf2, with N-acetylcysteine, PI-3K antagonist LY290042, and dominant-negative Akt abrogating the effects. Furthermore, celecoxib-induced HO-1 was inhibited by dominant-negative Nrf2. The functional significance of HO-1 induction was revealed by celecoxib-mediated inhibition of VCAM-1 expression, a response reversed by the HO-1 antagonist zinc protoporphyrin. HO-1 induction provides a molecular mechanism for clinical observations indicating relative freedom from atherothrombotic complications in patients taking celecoxib compared to other NSAIDs with comparable anti-inflammatory activity.

Statin-Induced Increase in HDL-C and Renal Function in Coronary Heart Disease Patients

Background: Little is known about the potential of statin-induced high-density lipoprotein cholesterol (HDL-C) increase to improve renal function in coronary heart disease (CHD) patients.

Role of NOD2/CARD15 in coronary heart disease.

Background:Bacterial DNA has been repeatedly detected in atheromatous lesions of coronary heart disease (CHD) patients. Phylogenetic signatures in the atheroma lesions that are similar to those of bacterial biofilms on human barrier organs, including the respiratory or gastrointestinal tract, raise the question of a defective barrier function in CHD. NOD2 plays a major role in defense against bacterial invasion. Genetic variation in the CARD15 gene, which encodes NOD2, was previously shown to result in a barrier defect that causes chronic inflammatory disorders (e.g. Crohn disease). In the present study, we investigated the possible involvement of NOD2/CARD15 in the pathology of CHD by i) analyzing the local expression of NOD2 in atherectomy versus healthy tissue (n = 5 each) using histochemical immunofluorescence and ii) by testing the three major functional CARD15 variants (R702W, G908R and 1007fs) for association with early-onset CHD in 900 German patients and 632 healthy controls.Results:In atherectomy tissue of CHD patients, NOD2 was detected in inflammatory cells at the luminal sides of the lesions. However, the allele and genotype frequencies of the three major CARD15 polymorphisms did not differ between CHD patients and controls.Conclusion:The NOD2 up-regulation in atheroma lesions indicates an involvement of this protein in the pathology of CHD. Although NOD2 could be important in local immune response mechanisms, none of the analyzed CARD15 variants seem to play a significant role in the etiology of CHD.

Statin-Induced Increase in HDL-C and Renal Function in Coronary Heart Disease Patients§

BackgroundLittle is known about the potential of statin-induced high-density lipoprotein cholesterol (HDL-C) increase to improve renal function in coronary heart disease (CHD) patients.Methods and Results In thispost hocanalysis of the GREek Atorvastatin and Coronary heart disease Evaluation (GREACE) Study we investigated the effect of HDL-C increase after statin treatment on renal function. From a total of 1,600 patients, 880 were on various statins (mainly atorvastatin) and 720 were not. Other secondary prevention therapies were similar in the 2 groups. After a 3 year follow up, the lipid profile was unchanged in the statin untreated group and estimated glomerular filtration rate (eGFR) was reduced by 5.1% compared with baseline (P<0.0001). In contrast, in the statin treated group non-HDL-C was reduced by 43%, HDL-C was increased by 7% and there was a significant increase in eGFR compared with baseline by 9.8% (P<0.0001). In multiple regression analysis, the mean 7% increase in HDL-C in the treated arm during the entire study was associated with a 5.6% increase in eGFR recorded after the 6th week of treatment. The odds ratio of eGFR increase with every 5% statin-induced rise in HDL-C was 1.78 (95% confidence interval 1.19-3.34; P=0.001).ConclusionsStatin treatment significantly improved renal function. Statin-induced HDL-C increase significantly and independently contributed to this improvement. This finding supports the concept that improving lipid variables other than low density lipoprotein cholesterol is also beneficial to preserving renal function.

Effect of probucol on vascular endothelial function of the coronary heart disease in the elderly

目的 观察丙丁酚(普罗布考)对冠心病血管内皮功能的影响.方法采用高分辨率超声诊断系统检测35例确诊冠心病的老年患者服用普罗布考前后肱动脉血流介导的舒张功能(即内皮依赖性舒张功能,FMD)和硝酸甘油介导的舒张功能(非内皮依赖性舒张功能,NMD)的变化,同时检测治疗前后血浆一氧化氮(NO)、内皮素(ET)水平的变化,并与28例未接受调脂治疗的老年冠心病患者进行对照研究.结果接受普罗布考治疗的患者ET、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)水平明显降低,而NO和FMD明显增加,NMD无显著性改变.结论普罗布考在降脂的同时能够改善老年冠心病患者血管内皮功能,且该作用独立于高密度脂蛋白胆固醇(HDL-C)水平的降低。

Applying ultrasonic-cardiography to detect left ventricular systolic and diastolic function in coronary heart disease

目的 探讨超声心动图对冠心病(CHD)患者左室功能的检测.方法收集因临床诊断为冠心病或疑诊冠心病而行冠状动脉造影(CAG)的170例患者,且均在同期内(间隔小于2周)行超声心动图检查,分为两组,其中冠心病患者89例,对照组81例,应用二维、M型及多普勒超声检测其左室容量变化及左室瓣口血流情况,据此判断左室的收缩舒张功能,并进行比较.结果冠心病患者的左室收缩和舒张功能指标较对照组有显著差异(P＜0.05,P＜0.01).结论超声心动图心功能指标能较好地评估冠心病患者的心功能状态。

Effect of a cardiac rehabilitation program on left ventricular diastolic function and its relationship to exercise capacity in patients with coronary heart disease: Experience from a randomized, controlled study

Background A cardiac rehabilitation and prevention program (CRPP) is a recognized nonpharmacological modality in the management of coronary heart disease (CHD). However, the effect of a CRPP on systolic function of the heart is controversial, and no data exists on diastolic function in CHD. A randomized, controlled study was conducted to address these issues. Methods Patients (n = 269) with recent acute myocardial infarction (n = 193) or after percutaneous coronary intervention (PCI) (n = 76) were randomized to either CRPP (2-hour twice-weekly exercise program for 8 weeks) or conventional therapy (control group). Serial treadmill exercise testing and at-rest echocardiography were performed during phases 1 (baseline), 2 (post–exercise training), and 3 (8-month follow up). Results The prevalence of left ventricular (LV) abnormal relaxation pattern (ARP) of diastolic dysfunction was increased in the control group only in phase 3 (65% vs 88%, χ 2 = 7.6, P < .01). Significant improvement of individual LV diastolic parameters towards less severe delayed relaxation was also observed in the CRPP group, especially in those with recent acute myocardial infarction or ARP. The gain in exercise capacity was faster and more substantial in the CRPP than the control group ( P < .001 for phase 2, P < .05 for phase 3), and was significantly correlated with LV diastolic indices in those with ARP. Exercise training had neutral effects on LV systolic function and rate-pressure product. Conclusions In patients with CHD, CRPP prevented the progression of resting LV diastolic dysfunction, without affecting systolic function. In those with ARP, the improvement of diastolic function predicted the gain in exercise capacity.

The correlation between high sensitivity C-Reactive Protein level and the Extent of Coronary Lesion and Cardiac Systolic Function in Coronary Heart Disease

To determine the mean value of high sensitivity C-Reactive Protein (hs-CRP), association between plasma level of hs-CRP with extent of disease and systolic function. A cross sectional study had been conducted to 106 coronary artery disease patients (90 stable angina pectoris, 11 unstable angina pectoris and 5 acute myocardial infarction). Plasma quantitative level of hs-CRP with cor angiography to determine extent of disease and ejection fraction were measured. The mean of hs-CRP levels in patients with SVD were 5,5 ± 7,6 mg/L, DVD were 6,6 ± 21,7 mg/L and TVD were 5,5 ± 8,0 mg/L and p=0,056, respectively. There were no significant association between hs- CRP levels with extent of disease. Systolic function had negative correlation with levels of hs-CRP (p=0,015, r=-0,235). This study showed that plasma level of hs-CRP cannot reflect the extent of disease, and it had negative correlation with systolic function. (Med J Indones 2003; 12: 201-6)

Coronary Heart Disease Risk Factors and LDL Cholesterol-Lowering Efficacy of Fibrates and Simvastatin

The objective of this study was to assess the low-density lipoprotein cholesterol (LDL-C) lowering efficacy of fibric acid derivatives (fibrates) and simvastatin as a function of coronary heart disease (CHD) risk status, stratified according to National Cholesterol Education Program guidelines. Two independent databases were analysed retrospectively. The first data set originated from a consecutive sample of 6340 patients with primary hypercholesterolaemia who completed the diet plus fibrate treatment phase of the Belgian General Practitioners Trial, an open-label, prospective study conducted in a primary care setting. The second data set was derived from 782 participants in five randomised, double-blind studies that each compared a specific fibrate with simvastatin. The main outcome measures were percentage of subjects reaching LDL-C treatment goal, and mean percentage reduction in LDL-C across 5 (first data set) or 3 (second data set) CHD risk strata. In the Belgian General Practitioners Trial, LDL-C lowering efficacy of fibrates was inversely related to CHD risk status as 15.0% of patients with prior CHD reached the LDL-C goal < 4.13 mmol/L(< 160 mg/dl) vs 30.2% of those without CHD and no other risk factor (p < 0.0001 after adjustment for baseline LDL-C and triglycerides). Adjusted mean percentage reductions in LDL-C were 15.1 and 18.2 in these strata, respectively (p < 0.05). Younger age, male gender, high blood pressure, low high-density lipoprotein cholesterol, and history of prior CHD were significant (p < 0.05) negative determinants of both outcome measures in multivariate analyses that adjusted for other risk factors. In the pooled analysis of five randomised trials, the percentage of fibrate-treated patients with prior atherosclerotic disease reaching LDL-C goal < 4.20 mmol/L (< 162 mg/dl) was significantly lower when compared with those without CHD and no risk factor other than LDL-C (adjusted odds ratio = 0.46; p = 0.009), while simvastatin efficacy was similar across CHD risk strata. In conclusion, our results, derived from two independent databases, suggest that the LDL-C lowering efficacy of fibrates, but not of simvastatin, is inversely related to CHD risk status. This exploratory analysis must be confirmed by future prospective studies.

Platelet Function During Ticlopidine and Eicosapentaenoic Acid Administration in Patients with Coronary Heart Disease

Antiplatelet drugs have been reported to be useful in unstable angina. This study was designed to investigate the effects of simultaneous administration of ticlopidine and eicosapentaenoic acid (EPA) on platelet function in coronary heart disease (CHD) patients. Ticlopidine significantly reduced platelet aggregation induced by ADP and collagen with no effect on arachidonate metabolism. The aggregation responses to collagen, ADP and arachidonate were not altered significantly by EPA (as fish oil) intake whereas thromboxane A(2) formation was reduced, but not completely inhibited. Combined therapy seems to achieve a more marked degree of inhibition of aggregation together with a fall in the urinary excretion of 11-dehydrothromboxane B(2) metabolite. Therefore, in CHD patients ticlopidine therapy plus fish oil administration could be useful to inhibit two different mechanisms (TxA(2)- and ADP-dependent) of platelet activation.

Hemodynamic benefits of synchronized 1:1 atrial pacing during sustained ventricular tachycardia with severely depressed ventricular function in coronary heart disease

The hemodynamic effects of atrial pacing were studied in 8 patients who had ventricular tachycardia (VT) during electrophysiologic testing. These patients had chronic recurrent VT associated with organic heart disease and depression of left ventricular function (ejection fraction = 0.23 to 0.35). Hemodynamic variables were recorded during sinus rhythm (58 to 103 beats/min), pacing-induced VT (133 to 214 beats/min) and synchronized 1:1 triggered atrial pacing (atrium paced, ventricle sensed and triggered mode) during VT. For the latter, the ventriculoatrial coupling interval was adjusted to produce a maximal blood pressure response; the optimal interval was observed to be between 60% and 73% of the RR interval. Mean arterial blood pressure decreased after the onset of VT (90 ± 11 to 79 ± 14 mm Hg, p < 0.05) but increased again when atrial pacing was added, to 98 ± 12 mm Hg. Cardiac index decreased during VT (2.2 ± 0.5 to 1.8 ± 0.5 liters/min/m 2 p < 0.05), but in each case improved by the addition of atrial pacing, to 1.9 ± 0.5 liters/min/m 2. Evidence from pressure recordings suggested that optimal atrial pacing resulted in atrial contraction in early left ventricular diastole. Thus, appropriately timed atrial pacing during VT can result in significant increases in blood pressure and a consistent increase in cardiac index. In addition to offering insight into the mechanisms of hemodynamic compromise during VT, the clinical use of this technique may be to improve hemodynamic values in patients with hemodynamically unstable VT.

Effects of atrial pacing on global and regional left ventricular function in coronary heart disease assessed by digital intravenous ventriculography

Digital i.v. ventriculography in conjunction with rapid atrial pacing was used to assess the effects of ischemic stress on global and regional function in 22 patients referred for cardiac catheterization (5 had normal coronary arteries and 17 had > 70% diameter reduction of at least 1 major coronary artery). End-diastolic, end-systolic and stroke volume indexes and the ejection fraction were determined by an area-length technique from the mask mode images before and after pacing. In addition, segmentar responses were quantitated using a radial shortening method. Subjects with normal coronary arteries showed no overall change in the postpacing volume or ejection fraction indexes. Coronary patients showed no overall change in postpacing end-diastolic volume (86 ± 25 ml/m 2 at control vs 90 ± 31 ml/m 2 after pacing, difference not significant), but there was a significant increase in endsystolic volume (25 ± 15 ml/m 2 at control vs 32 ± 18 ml/m 2 after pacing, p < 0.005) and a decrease in ejection fraction (72 ± 11% at rest vs 64 ± 18% after pacing, p < 0.025). Furthermore, quantitative deterioration in wall motion was seen in 14 of 17 coronary patients (82%) and in none of the normal patients. Analysis of segmental wall motion was the most sensitive diagnostic Variable. A combination of atrial pacing stress testing and digital i.v. ventriculography is useful in detecting functionally significant coronary disease through quantitation of global and regional dysfunction which does not require arterial cannulation.

The Electrocardiogram as an Index of Left Ventricular Function in Coronary Heart Disease

To determine the utility of conventional electrocardiographic criteria for the assessment of left ventricular function, we applied pre-determined criteria to the analysis of the ECGs of 171 patients with chronic coronary disease. Eighty patients had no criteria for infarction. Seventeen had a criterion for anterior, 59 a criterion for inferior, three for strict lateral, four for true posterior and eight for combined infarction. Of the 59 with inferior infarction, 25 had QaVF greater than or equal to 0.03 sec. These 25 together with the 25 with anterior or combined infarction constituted a subgroup of 50 patients which included 35 of the 44 (80 percent) of those with an ejection fraction less than 0.50. Among the remaining 121, only nine (7 percent) had a depressed ejection fraction. Thus, the ECG criteria identified correctly 147 (86 percent) patients with regard to the presence or absence of left ventricular dysfunction.