ECG Signs Of Myocardial Ischemia Research Articles

415 DOES MYOCARDIAL BRIDGING TRIGGER MYOCARDIAL ISCHEMIA?

Abstract Background Myocardial bridging (MB) is a congenital epicardial coronary abnormality, in which a segment of the artery runs through the myocardium, determining dynamic stenosis during systole. Whether MB can be responsible by itself for myocardial ischemia remains unclear. Thus, we aimed to evaluate whether the dynamic stenosis related to MB can cause signs and symptoms of myocardial ischemia. Methods We enrolled 41 consecutive patients who underwent coronary angiography because of chest pain suspected for ischemic heart disease and were found to have MB in the absence of any significant flow-limiting coronary stenosis and any other cardiac disease. A group of 14 patients who also underwent coronary angiography because of chest pain suspected for ischemic heart disease, but found to be free of any coronary or cardiac abnormality (including MB) and also showed negative results at exercise stress test (EST) served as controls. All enrolled patients underwent a maximal treadmill EST according to standard Bruce protocol. A complete echocardiographic examination was performed at rest and at peak exercise. Results Baseline EST parameters were comparable between groups, whereas peak diastolic blood pressure (pDBP) was slightly higher in the MB group (p=0.044). No clinically significant differences were found in baseline echocardiographic parameters, although the E wave deceleration time (DcT) was longer (p=0.038) and global longitudinal strain (GLS) was higher (p=0.05) in the MB group. During exercise, left ventricular ejection fraction (LVEF) improved significantly in both groups (p<0.001), without any difference between the 2 groups. GLS did not show any significant changes with exercise in both groups. Moreover, among MB patients, no differences were found in stress echocardiographic results between those with positive vs. those with negative EST. Conclusions We failed to demonstrate any significant ischemic impairment of LV systolic and diastolic function at maximal EST in patients with MB. Moreover, we also failed to demonstrate any LV dysfunction in MB patients that developed ECG signs of myocardial ischemia during EST, as compared to those without evidence of myocardial ischemia. Thus, our data question about the ability of MB itself to trigger significant myocardial ischemia in clinical practice.

Cystatin C and Chronic Complications of Diabetes Mellitus in a Subsaharian Population

Background: Type 2 diabetes (T2D) is a chronic and progressive condition whose early management is crucial in preventing the occurrence of its chronic degenerative complications. Cystatin C (CysC) is a biomarker that may have a beneficial interest in the early detection of microvascular and macrovascular complications of T2D. Methods: We carried out a cross-sectional analytic study at the National Obesity Center of the Yaounde Central Hospital. We recruited 135 patients with T2D and performed a neurologic physical exam using the Toronto clinical score, a fundoscopy, ECG, ABI, and the following paraclinicals: dosage of serum levels of Cystatin C, lipid profile (with determination of Atherogenic indexes), Creatinine (with calculation of glomerular filtration rate using CKD-EPI formula) and hs-CRP. Results: Prevalences of diabetic retinopathy, nephropathy, neuropathy and PAD were 3.0%, 8.9%, 38.5%, 28.1% respectively. Electrocardiographic signs of myocardial ischemia were present in 5.9 % of the participants. We found 0.3[0.5-0.3] mg/l as median levels of the HDL-cholesterol and 0.9[1.2-0.7] mg/l for LDL-cholesterol. The median value of GFR was 105.7[119,0-85.7] ml/min/1.73m². The median serum CysC level was 0.8[0.9-0.6]mg/l and varied with age (p=0.01), A1C (p=0.016) and high blood pressure (HBP) (p=0.006). There was a relationship between serum CysC and diabetic nephropathy (p=0.01) and neuropathy (p=0.025). There was no significant relationship with diabetic retinopathy (p=0.225), PAD (p=0.169) and ECG signs of myocardial ischemia (p=0.669). Conclusion: Chronic microvascular and macrovascular complications of type 2 diabetes are common and in our study are predominantly represented by diabetic neuropathy and PAD. Serum CysC can be useful in the diagnosis of chronic complications of T2D.

Challenges of Diagnosing Congenital Heart Defects — Anomalous Origin of the Left Coronary Artery from the Pulmonary Artery

Background. Anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA) also known as Bland — White — Garland syndrome is a rare congenital heart defect that affects 1 in every 300 000 newborns, thus comprising 0.22% of all congenital heart defects and 0.4–0.7% of critical congenital heart defects. In case of a more favorable disease course, symptoms typically appear between the 1st and 2nd months after birth. The ECG may show typical signs of ischemia, myocardial infarction, and left ventricular hypertrophy. The EchoCG is more informative as it enables the visualization of coronary artery orifices. Surgical correction is the only treatment method for this heart defect.Case report.Patient G.S.V., one month of age, was admitted to the neonatal pathology unit. Based on the physical examination the patient’s condition was severe. The skin was pale with cyanosis of the nasolabial triangle. The respiration rate was accelerated (50–52 breaths per minute) with the indrawing of the intercostal spaces. The displacement of the apex beat 1 cm to the left of the left midclavicular line was revealed by palpation. The displacement of the left border of the relative cardiac dullness to the anterior axillary line was revealed by percussion. Upon auscultation, the first heart sound at the heart apex was decreased, and there was a blowing systolic murmur radiating to the left anterior axillary line. Upon examination the child was diagnosed with severe acute acquired non-rheumatic diffuse viral bacterial carditis. The lack of improvement in the child’s condition following the myocarditis treatment and the examination results were suggestive of the anomalous coronary artery. The child was transferred by emergency to the Penza Federal Center of Cardiovascular Surgery where the diagnosis was confirmed.Conclusion. Despite being rare, this congenital heart defect may be diagnosed in clinical pediatric practice. A thorough record of complaints and medical history is an important step in its early diagnosis, and the presence of signs of heart failure requires additional examination. In case of suspected myocardial lesions, presence of high troponin levels and other markers of myocardial injury in the blood, ECG signs of myocardial ischemia and lack of improvement despite the treatment conducted, pathologic changes in the coronary arteries must be ruled out.

Questions of the mathematical modeling of the progression of coronary heart disease in patients with type 2 diabetes mellitus

In 2017-2019, 40 patients were examined (16 of them men, 24 women) with type 2 diabetes mellitus in combination with IHD, of which 38 patients had a favorable course and 8 with an unfavorable course. For an unfavorable profile, the presence of strokes, mycocardial infarction (fatal, nonfatal), repeated hospitalizations for worsening chronic heart failure (decrease in ejection fraction), repeated surgical interventions (percutaneous coronary intervention, coronary artery bypass grafting) for the current 3 years was taken into account. The average age of patients was 65.5 years. In total, 119 signs recorded in the first three days from the moment of patient's arrival were analyzed as possible predictors of an unfavorable prognosis. From this whole set, a number of parameters with corresponding values ​​were selected as markers of coronary heart disease, which showed the highest incidence rate in the group of patients with adverse course (NBT) and the highest in the group of patients with favorable course (BT). the most pathognomonic predictors of IHD progression in patients with type 2 diabetes were systolic LV dysfunction (fv <40%), SBP> 160 mm Hg and/or DBP above 100 mm Hg. Art., severe angina pectoris, LVH and ECG signs of myocardial ischemia, persisting upon discharge from the hospital, history of ACVA comorbidity plus DM-2.

Myocardial regeneration strategy using Wharton’s jelly mesenchymal stem cells as an off-the-shelf ‘unlimited’ therapeutic agent: results from the Acute Myocardial Infarction First-in-Man Study

IntroductionIn large-animal acute myocardial infarction (AMI) models, Wharton's jelly (umbilical cord matrix) mesenchymal stem cells (WJMSCs) effectively promote angiogenesis and drive functional myocardial regeneration. Human data are lacking.AimTo evaluate the feasibility and safety of a novel myocardial regeneration strategy using human WJMSCs as a unique, allogenic but immuno-privileged, off-the-shelf cellular therapeutic agent.Material and methodsThe inclusion criterion was first, large (LVEF ≤ 45%, CK-MB > 100 U/l) AMI with successful infarct-related artery primary percutaneous coronary intervention reperfusion (TIMI ≥ 2). Ten consecutive patients (age 32–65 years, peak hs-troponin T 17.3 ±9.1 ng/ml and peak CK-MB 533 ±89 U/l, sustained echo LVEF reduction to 37.6 ±2.6%, cMRI LVEF 40.3 ±2.7% and infarct size 20.1 ±2.8%) were enrolled.Results30 × 106 WJMSCs were administered (LAD/Cx/RCA in 6/3/1) per protocol at ≈ 5–7 days using a cell delivery-dedicated, coronary-non-occlusive method. No clinical symptoms or ECG signs of myocardial ischemia occurred. There was no epicardial flow or myocardial perfusion impairment (TIMI-3 in all; cTFC 45 ±8 vs. 44 ±9, p = 0.51), and no patient showed hs-troponin T elevation (0.92 ±0.29 ≤ 24 h before vs. 0.89 ±0.28 ≤ 24 h after; decrease, p = 0.04). One subject experienced, 2 days after cell transfer, a transient temperature rise (38.9°C); this was reactive to paracetamol with no sequel. No other adverse events and no significant arrhythmias (ECG Holter) occurred. Up to 12 months there was one new, non-index territory lethal AMI but no adverse events that might be attributable to WJMSC treatment.ConclusionsThis study demonstrated the feasibility and procedural safety of WJMSC use as off-the-shelf cellular therapy in human AMI and suggested further clinical safety of WJMSC cardiac transfer, providing a basis for randomized placebo-controlled endpoint-powered evaluation.

Diagnostic ECG du syndrome coronarien aigu

This review updates the clinician to the many typical, but also underappreciated and subtle, ECG signs of myocardial ischemia and infarction. This compilation explains the dynamic changes during severe myocardial ischemia (schematically, abnormal T-wave then ST-segment and QRS complex) and illustrates in detail the heterogeneity of the ECG representations. It emphasizes the importance of seeking any abnormality in the T-wave (amplitude or polarity not conforming to QRS, symmetry at the base), ST-segment (excessive elevation, minimal depression, or loss of appropriate discordance), but also within the QRS complex, to check whether the baseline ECG is normal or affected by frequent abnormalities (ventricular hypertrophy, bundle-branch block…).

Phase I clinical evaluation of ZD6126, a novel vascular-targeting agent, in patients with solid tumors

ZD6126 is a novel vascular-targeting agent that disrupts the endothelial tubulin cytoskeleton causing selective occlusion of tumor vasculature and extensive tumor necrosis. This Phase I clinical study was conducted to evaluate the dose and administration schedule of ZD6126. Adult patients with solid tumors refractory to existing treatments received a 10-min, single-dose intravenous infusion of ZD6126 every 14 or 21 days. Subsequent dose escalation was performed, based on the incidence of adverse events (AEs) within the first cycle of drug administration. Blood samples were obtained for pharmacokinetic analysis, and the effects of ZD6126 on tumor vasculature were visualized using DCE-MRI technology. Forty-four patients received ZD6126 (5-112 mg/m2 in the 21-day schedule, n=35; 40-80 mg/m2 in the 14-day schedule, n=9). Common AEs were similar in both groups and included abdominal pain, nausea and vomiting, which appeared to be dose related. The incidence of abdominal pain at 112 mg/m2 in the 21-day study prevented further dose escalation. Pharmacokinetic studies confirmed that ZD6126 is rapidly hydrolyzed to ZD6126 phenol. There was no difference in the pharmacokinetics of ZD6126 phenol upon repeat administration or between the two dosing regimens. DCE-MRI evaluation has demonstrated the antivascular effects of ZD6126. This study identified that ZD6126 administered every 2 or 3 weeks at 80 mg/m2 was well tolerated, with mild but manageable gastrointestinal AEs. In approximately 11% (5 out of 44) of patients, ZD6126 was associated with cardiac events categorized as dose limiting toxicities (one patient with asymptomatic decreased left ventricular ejection fraction (LVEF), two with increased troponin concentrations, one with myocardial ischemia, and one with ECG signs of myocardial ischemia).

Myocardic extended ischemia after scombroid syndrome

We describe a case of a healthy woman, presenting to the emergency department because of sudden onset of diffuse pruriginous erythema, profound arterial hypotension and anginal chest pain, just after consuing a meal with cooked fresh tuna fish. She developed progressive ECG signs of myocardial ischemia suggesting subendocardial infarction and increased serum level of troponin I. After vigourous fluid resuscitation with iv fluids and treatment with anti-hystamine drugs, corticosteroids, beta-blockers and calcium-channell blockers she progressively recovered. A clinical diagnosis of sgombroid syndrome was established: it is a syndrome which may follow the ingestion of some spoiled fish, characterized by urticara, headhache, gastrointestinal upset and rarely bronchospasm, shock, coronary ischemia and arrythmias. A sample of the consumed fish could be analysed, finding a very high level of hystamine concentration, conferming the diagnosis of sgombroid syndrome. A coronary angiography was performed and confermed the patient had a normal coronary tree, devoid of atherosclerotic lesions. Her anginal symptoms and ECG signs were probably due to functional ischemia determined by hystamine mediated vasoconstriction and hypotension. This not so rare but not well known syndrome is further discussed and addressed to the emergency physicians’ attention, because of its importance in the differential diagnoses of suspected food allergies

Prognostic value of biochemical markers, 12-lead ECG and patient characteristics amongst patients calling for an ambulance due to a suspected acute coronary syndrome.

To evaluate whether a 12-lead ECG, together with a multi-marker strategy that used point-of-care measurements of myoglobin, creatine kinase (CK-MB) and troponin I, was able to predict patients at short- and long-term risk of death, when simultaneously considering age, gender, previous history, symptoms and clinical findings on arrival of the ambulance. Prospective observational study. Consecutive patients (n=511) in ambulances in Stockholm and Göteborg in Sweden who called for an ambulance due to chest pain or other symptoms raising a suspicion of acute coronary syndrome. In almost all patients, a diagnostic ECG, patient baseline characteristics and measurements of CK-MB, troponin I and myoglobin were recorded. In univariate analysis, the highest 30-day mortality (17%) was found amongst patients with the combination of ECG signs of myocardial ischaemia and the elevation of any biochemical marker. The highest 1-year mortality (20%) was found amongst patients with ECG signs of myocardial ischaemia and the elevation of any biochemical marker. Increasing age (RR 1.07; 95 CI 1.02-1.13) lack of symptoms of chest pain and a previous history of hypertension (3.02; 1.08-8.79) were independent predictors of 30-day mortality. Myoglobin was the only biochemical marker independently associated with 30-day mortality (6.66; 1.83-22.3). Increasing age (1.11; 1.06-1.16), previous history of diabetes (3.42; 1.41-8.25) heart failure (2.64; 1.26-5.52) and other symptoms than chest pain and dyspnoea (5.23; 2.14-12.76) were independent predictors of 1-year mortality. In many of the variables the confidence limits were wide. Amongst patients with a clinical suspicion of acute coronary syndrome, those with the combination of ECG signs of myocardial ischaemia and the elevation of any biochemical marker on arrival of the ambulance form a group with a particularly high risk of death. However, age as well as aspects of clinical history and type of symptoms independently contribute to prognostic information.

Effects of chronic beta-blockade on compensatory mechanisms during acute isovolaemic haemodilution in patients with coronary artery disease

We have compared compensatory mechanisms during acute isovolaemic haemodilution of 12 ml/kg body weight of blood with hydroxyethyl starch (450,000/0.7) exchange, in non-beta-blocked and beta-blocked patients with coronary artery disease. During haemodilution, mean concentrations of haemoglobin decreased from 12.8 (SEM 0.2) to 10.1 (0.1) g dl-1 (P < 0.01). Only beta-blocked patients had an increase in cardiac index (P < 0.01); in non-beta-blocked patients, cardiac index remained constant. In both groups oxygen extraction increased (P < 0.01), but the increase tended to be greater in non-beta-blocked patients (P = 0.06). Oxygen consumption was maintained in both groups. There were no ECG signs of myocardial ischaemia. We conclude that beta-blocked and non-beta-blocked patients with coronary artery disease tolerated well moderate haemodilution to a haemoglobin value of approximately 10 g dl-1, however, compensatory haemodynamic mechanisms differed fundamentally between the two groups.

Relation Between Myocardial Fractional Flow Reserve Calculated From Coronary Pressure Measurements and Exercise-Induced Myocardial Ischemia

Myocardial fractional flow reserve (FFRmyo) is a functional index of stenosis severity that can be derived from intracoronary pressure measurements performed during maximal vasodilatation. It is defined as the maximal myocardial perfusion during hyperemia in the presence of a stenosis in the epicardial artery expressed as a fraction of its normal maximal expected value. To determine threshold values of FFRmyo, of hyperemic translesional pressure gradient (delta P(max)), and of resting translesional pressure gradient (delta P(rest)) that are uniformly associated with exercise-induced ischemia, we studied the relation between these pressure-derived indexes and the results of exercise ECG. We studied 60 patients with an isolated lesion in one major epicardial coronary artery, normal left ventricular function, and no left ventricular hypertrophy. Maximal exercise ECG (off anti-ischemic medication) was performed within 6 hours before catheterization. Intracoronary pressure measurements were taken at rest and during hyperemia with a pressure monitoring guide wire. ST-segment depressions at peak exercise (considered abnormal when > or = 0.1 mV) were compared with FFRmyo, delta P(max), and delta P(rest). Thirty-seven patients had an abnormal and 23 patients a normal exercise ECG. A significant linear correlation was found between the magnitude of ST-segment depressions and both FFRmyo and delta P(max) (r = -.75, SEE = 0.53; r = .71, SEE = 0.56). A weaker correlation was noted between ST-segment depressions and delta P(rest) (r = .53, SEE = 0.67). Sensitivity and specificity curves were constructed for the prediction of an abnormal exercise ECG for the three pressure-derived indexes. The values that most accurately predicted an abnormal exercise ECG were 66% for FFRmyo, 31 mm Hg for delta P(max), and 12 mm Hg for delta P(rest). No patient with a FFRmyo value > 72% showed an abnormal exercise ECG. In addition, receiver operating characteristic curves demonstrated a greater accuracy of FFRmyo and of delta P(max) than of delta P(rest) for predicting the results of the exercise ECG. In the present study, cutoff values of FFRmyo and translesional pressure gradients are established from the relation between intracoronary pressure-derived indexes and ECG signs of myocardial ischemia during maximal exercise. These values can be helpful for clinical decision making in cases with dubious angiographic results. Furthermore, our data support the concept that stenosis physiology is better reflected by hyperemic than by basal measurements.

A comparison of pipecuronium with pancuronium on haemodynamic variables and plasma catecholamines in coronary artery bypass patients

Pipecuronium bromide, a new neuromuscular relaxant with steroidal structure, is devoid of effects on the autonomic nervous system and may be useful in patients where haemodynamic stability is mandatory. However, tracheal intubation may alter this haemodynamic profile. Therefore, we carried out a prospective double-blind study in 30 patients undergoing coronary artery bypass surgery with the purpose (1) of determining if intubation influenced the haemodynamic stability in patients paralyzed with pipecuronium and (2) of comparing plasma catecholamine concentrations after pipecuronium with those after pancuronium. Thirty patients were randomized into two groups receiving either pipecuronium 100 micrograms.kg-1 or pancuronium 150 micrograms.kg-1 after induction of anaesthesia with midazolam and fentanyl. Haemodynamic variables and plasma catecholamines were measured before and after induction, after the muscle relaxant three times and twice after intubation. After anaesthesia induction decreases in heart rate (HR), mean arterial pressure (MAP) and cardiac index (CI) were observed in both groups. These haemodynamic variables were unchanged after pipecuronium whereas after pancuronium HR increased from 53 +/- 11 b.min-1 to 64 +/- 9 b.min-1 after induction (P < 0.05) and CI from 2.5 +/- 0.5 L.min-1 to 3.0 +/- 0.8 L.min-1 (P < 0.05). Furthermore ECG signs of myocardial ischaemia appeared in four patients after pancuronium and the decay of plasma norepinephrine concentration was slower than with pipecuronium. We conclude that pipecuronium given after induction of anaesthesia is free of sympathomimetic or vagolytic activity and does not influence haemodynamic variables for up to ten minutes after tracheal intubation.

Protruding left ventricular thrombus formation following blunt chest trauma

in the event of myocardial ischemia, SACE increases markedly at maximum effort as well as during recovery. Our data on SACE activity in nonischemic subjects support similar results obtained by Milledge and Catley,” who found SACE to remain unchanged during extended stress testing (up to 60 minutes) in normal healthy subjects. In light of our findings, we propose that SACE elevation could reflect acute endothelial vascular damage (both in general and in particular in the cardiac vasculature) in subjects with clinical and ECG signs of myocardial ischemia during stress testing (regardless of the duration of exercise).

Treatment of Ischemic Heart Disease in the 1990s

During recent years, understanding of the basic pathology, pathophysiology, and morbid risk of ischemic heart disease has increased immensely, but a wide gulf still exists between such knowledge and its practical application to the individual patient. Although the treatment of ischemic heart disease continues to pose many dilemmas for the physician in the 1990s, the key issues are easy to define, particularly with regard to pharmacotherapy. The basic pathologic processes and their rate of development and progression, their pathophysiologic consequences, and their morbidity and mortality risks are becoming increasingly clear. Until methods are developed to reconstitute the obstructed coronary arteries, clinical attention must be directed primarily to alleviating symptoms and ECG signs of myocardial ischemia and improving the deranged hemodynamic disorder. These primary objectives are now achievable with modern anti-ischemic drugs such as nicorandil. With the availability of efficacious drugs against clinical symptoms, ECG signs, and hemodynamic associates of ischemic heart disease, clinical attention must be redirected to retardation or even regression of the primary myocardial ischemic syndrome. This therapeutic goal can be achieved only by correction of the secondary risk factors that are present in many patients with ischemic heart disease. Only by such a comprehensive approach, namely, that of treatment allied to prevention, can the gap between knowledge and its practical application to the individual patient be narrowed.(ABSTRACT TRUNCATED AT 250 WORDS)

Late streptokinase infusion and antithrombotic treatment in myocardial infarction reduce subsequent myocardial ischemia

Of 255 consecutive patients with acute myocardial infarction, 111 were eligible for attempted late thrombolysis. They were randomly assigned to either thrombolytic and antithrombotic treatment (treatment group) or routine treatment (control group). Patients in the treatment group received streptokinase initiated late (mean 32 hours; range 12 to 49) after the onset of symptoms, followed by heparin infusion for at least 5 days and warfarin and dipyridamole for at least 3 months. Patients were examined clinically and by bicycle ergometry on discharge from the hospital and after 3 and 12 months. The two groups did not differ with respect to deaths or reinfarctions. There was a trend toward a lower incidence of angina pectoris in the treatment group. Exercise tolerance in this group was significantly higher than in the control group (at 3 months 124 ± 39 W vs 107 ± 41 W; p < 0.05). The difference was entirely accounted for by patients with no previous history of infarction or angina pectoris (at 3 months 142 ± 37 W vs 112 ± 45 W; p = 0.01). ECG signs of myocardial ischemia, silent or symptomatic, occurred at significantly lower levels of exercise among patients in the control group compared with patients in the treatment group. The results support the notion that thrombolytic therapy given as late as 12 to 49 hours after the onset of symptoms may reduce the incidence of residual ischemia during the postinfarction period.

Effects of adenosine on renal function, central haemodynamics and ECG signs of myocardial ischaemia, after coronary artery bypass surgery

Effects of adenosine on renal function, central haemodynamics and ECG signs of myocardial ischaemia, after coronary artery bypass surgery

Effects of nitroglycerin and nifedipine on coronary and systemic hemodynamics during transient coronary artery occlusion

Nitroglycerin (NTG) and nifedipine (NIF) have the potential to augment coronary blood flow in addition to reducing peripheral determinants of myocardial oxygen demand as a synergistic protective mechanism during ischemia. To examine these effects, systemic and coronary hemodynamic responses were measured continuously before and during brief periods of myocardial ischemia induced by left anterior descending coronary balloon occlusion in 26 patients undergoing angioplasty (PTCA). Data were compared for two matched occlusion periods, one control and one “drug” occlusion. In 17 patients (NTG group), 200 μg of intracoronary NTG was given immediately before coronary occlusion. In nine patients (NIF group), 10 mg of sublingual NIF was given 15 minutes before the “drug” occlusion. NTG significantly but transiently reduced mean arterial pressure (91 ± 11 to 82 ± 15 mm Hg, p < 0.05) and augmented basal coronary blood flow (95 ± 38 to 127 ± 54 ml/min, p < 0.05) but did not alter great vein blood flow (59 ± 29 vs 61 ± 29 ml/min) or coronary occlusion pressure (25 ± 7 to 24 ± 7 mm Hg) during ischemia. NIF significantly reduced systolic, diastolic, and mean arterial pressure (119 ± 21 to 95 ± 8 mm Hg, p < 0.001) and heart rate-pressure product from control. NIF maintained basal great vein blood flow (125 ± 41 to 106 ± 57 ml/min) during reduced myocardial oxygen demand, but did not affect great vein blood flow (73 ± 29 to 79 ± 37 ml/min) or coronary occlusion pressures during ischemia. Neither agent prolonged the time to ischemic ST segment alteration after the 50 to 60 second coronary flow occlusion periods. These data suggest that during the initial minutes of myocardial ischemia due to coronary occlusion, neither the coronary nor peripheral hemodynamic effects of the two vasodilators significantly improved regional coronary blood flow responses of ECG signs of myocardial ischemia. During PTCA, the beneficial effects of these agents most likely occur through mechanisms such as spasmolytic action, or indirectly by reduction of myocardial oxygen demand, more than directly augmenting coronary blood flow or collateral supply.

Prevalence of cardiac and aortic enlargement in rheumatoid arthritis and its relationship to some characteristics of the patients. A radiological and clinical study.

The chest radiographs of 309 patients with rheumatoid arthritis (RA) were compared with those of 309 controls matched for sex and age. Cardiac enlargement was more frequent in RA females than in controls (P less than 0.05) and the frequency of aortic shadow enlargement was higher in RA patients aged greater than or equal to 60 years than in controls (P less than 0.05). Both cardiac and aortic enlargement was significantly related to several parameters of the severity and the activity of RA, corticosteroid therapy, and elevated blood pressure. A high mortality was present in patients with aortic enlargement and in patients with ECG signs of myocardial ischaemia.

The effect of pindolol, a beta-receptor blocking agent, in heart rate and blood-pressure during submaximal and maximal exercise

The effect of a new beta-receptor blocking agent, 4-2 (2-hydroxy-3-isopropylaminopropoxy)-indole, pindolol (Visken®), was investigated in patients with essential hypertension of WHO grades I–II. Maximal and submaximal working capacity tests were done before and during treatment in 30 patients. 15 patients underwent a double-blind cross-over trial with placebo; and a further 15 patients were examined in an open study including a multiscaled working capacity test. The work tests were performed on a bicycle ergometer with increasing loads. The ECG was recorded continuously, and the blood-pressure was measured with a cuff. — In both groups the heart rate and systolic blood-pressure decreased significantly during treatment with Visken, both at rest and during exercise. The resting and post-exercise diastolic blood-pressures were also significantly reduced after beta-receptor blockade with Visken. No ECG signs of myocardial ischemia were found. The work capacity tests showed a slight reduction, of about 100 kpm/min, in four patients, whilst three improved their maximal working capacity.