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Sixteen male patients with typical angina pectoris secondary to coronary atherosclerosis performed two daily standardized exercise tests during two consecutive days. Three hours before each exercise they received placebo or 400 mg practolol administered orally in double-blind fashion in order to complete a cross-over design. Practolol significantly prolonged the exercise duration by 30.6% and delayed the appearance time of ischaemic electrocardiographic changes by 67.7%. Maximal heart rate, systolic pressure, and pressure-rate product were also reduced after medication. In order to investigate further the effects of this beta blocking agent, myocardial function and metabolism at rest and during supine exercise were assessed in 12 male patients with coronary artery disease before and after practolol 30 mg, iv. At rest, practolol produced a decrease in tension-time index (18%), cardiac index (17%), heart rate (10%), and stroke index (7%). A significant reduction was also observed in resting stroke work index (14%) and systolic and mean aortic pressure (6%). Left ventricular end-diastolic pressure remained unchanged. During supine exercise, only time-tension index (12%), heart rate (12%), and cardiac index (10%) were significantly reduced after the beta blocking agent. Practolol did not significantly change the arterial glucose, lactate, inorganic phosphate, potassium, calcium, magnesium, pH, PCO2, or PO2. The beta blocking agent did not modify the myocardial extraction of any of these substrates at rest or during exercise. In the dosage used in both studies, practolol significantly improved the exercise tolerance and reduced the ischaemic manifestations. The efficacy of practolol in angina pectoris may result mostly from its ability to decrease heart rate and systolic pressure during exercise.

To assess the prognosis of patients with a strongly positive exercise ECG, the 5-year cumulative survival rate was computed for 220 medically treated patients. Of these patients, 107 had coronary angiograms (group A) and 113 did not (group B). All had horizontal or downsloping ST depression greater than or equal to 2 mm during a multistage Bruce protocol treadmill exercise test. In group A, the overall 5-year survival rate was 74 +/- 5%. Survival decreased with decreasing duration of exercise: All patients who achieved stage IV (541 seconds or more) survived, whereas the survival rate was 86 +/- 6% when the patients terminated their exercise during stage III (361 - 540 seconds), 73 +/- 7% when during stage II (181 - 360 seconds) and only 52 +/- 13% when during stage I (180 seconds or less). The mortality was associated with more severe coronary artery disease, and sudden death was the main cause of death. Patients in group B had a longer mean exercise duration than those in group A and, as expected, a higher survival rate (91 +/- 3%, p less than 0.01), which also varied according to the exercise duration. Among patients with a strongly positive exercise ECG, the duration of exercise identifies subsets that have different survival rates.

Morphological and biochemical observations from our laboratory have shown the presence of lipids in the cardiac interstitial spaces of the dog. The present study was designed to assess the importance of free fatty acids (FFA) in these lipids using FFA or sucrose tracers in 14 anesthetized fasting open-chest mongrel dogs. Endogenous FFA and labeled tracers were measured in arterial and coronary sinus plasma; they were also determined in lymph collected from cardiac efferent lymphatic trunks. [14C] sucrose was infused at a constant rate in the femoral vein of 5 dogs. The concentration of the tracer in the lymph was 90% of the arterial concentration after 60 min of infusion. On the other hand, when [1-14C] palmitate was infused at the same rate in 7 dogs, the ratio of lymph to arterial tracer concentration was only 20% (60 min) and 25% (120 min), even though the myocardial extraction and oxidation of the tracer were stable. This ratio tended to reach a plateau (greater than or equal to 90%) only 24 hr after a bolus injection of the tracer. This tracer study shows the presence of a pool of myocardial fatty acids with a relatively slow turnover rate that may constitute an important reservoir of FFA.

There is still controversy as to which characteristics of the pressure-volume relation should be used to define myocardial contractility. In the present study a mathematical model for the left ventricle as a two-dimensional cylinder contracting radially and symmetrically was used to establish a relation between a calculated intramyocardial pressure (Dh) and the P-V relation (PVR) at end-systole. Four new indices are introduced that allow a better assessment of change in inotropic state of the myocardium, namely the calculated intramyocardial pressure (Dh), the calculated resultant pressure across the inner surface of the myocardium (Dh-P) (P = cavity pressure), the work Wt related to the pressure (Dh) and the work Wd related to the pressure (Dh-P). A relation between Wt and Wd and different parts of the area under the PVR is established. Indices derived in this manner from the PVR to study changes in myocardial contractility appear to have a clear physical meaning.

Free fatty acids (FFA) have been shown to be a major myocardial substrates during the postabsorptive state in humans. In order to document the utilization of these substrates by the heart while heparin was infused, the following study was designed. During heparin infusion, total and individual FFA were measured in arterial and coronary sinus plasma during the postabsorptive state in 13 patients with coronary artery disease and in 4 patients with no evidence of cardiac disease. Oleic-1-14C acid bound to albumin was infused at a constant rate for at least 7 min into the left coronary artery. Left coronary blood flow was determined in all patients. It was assumed the oleic-1-14C acid behaves like endogenous FFA. Arterial FFA concentration was high (mean and SEM: 1 +/- 0.21 mumoles/ml) and varied by less than 10% during the course of the study in 14 of the 17 patients. Oleic acid constituted 44% of all arterial FFA. The relative concentrations of the various individual FFA were similar in arterial and coronary sinus plasma. The average FFA extraction was 19.9 +/- 2.1%. In contrast, the oleic-1-14C acid extraction was relatively more steady during the infusion, and the mean extraction of this tracer was 36.0 +/- 2.1%. Myocardial uptake for the entire group was 52.3 +/- 6.3 mumoles/min. Although a definite plateau for 14CO2 release from oleic-1-14C acid oxidation was not obtained, at least 31.8 +/- 4.3% of the removed FFA was oxidized, representing 49.3 +/- 6.4% of myocardial oxygen consumption. The failure of oleic-1-14C acid oxidation to reach a steady state was not due to delay in the myocardial CO2 pool, since 14CO2 release from infused NaH 14CO3 and lactate-1-14C in 11 other subjects revealed that in equilibrium was obtained within 5 min. These findings indicate that the generation of 14CO2 from oleic-1-14C acid oxidation is relatively slow, and the uptake of labeled FFA is partly matched by release of unlabeled FFA, suggesting that the human heart has important lipid pools.

In an attempt to retrain family doctors in hypertension and hyperlipoproteinemia, computer assisted instruction (CAI) was assessed in fourteen doctors (Group 1) and its efficiency was compared to that of traditional lectures given to twenty-one doctors (Group 2). The same objectives, contents and illustrations were used in both teaching approaches. There was no significant difference for age, year of graduation and type of practice in the two groups. Comparison between pre-test and immediate post-test revealed a significant gain of knowledge for hyperlipoproteinemia (group 1, 33% and group 2, 22%) and hypertension (group 1, 16% and Group 2, 19%). A year later a similar post-test was done in both groups, and no significant difference was found between this late post-test and the pre-test. CAI applied to family doctors is as efficient for learning as traditional lectures, and both approaches failed to show retention of knowledge after one year. This is perhaps the result of having selected instructional objectives of theoretical more than practical value.

During an atrial pacing test, a correlative study in myocardial lactate, glucose, potassium, and inorganic phosphate balances was done in 34 patients with clinical evidence of ischemic heart disease. Electrocardiogram was continuously monitored while left ventricular end-diastolic pressure (LVEDP) was measured before and immediately after pacing. Coronary angiograms performed after the pacing test revealed atherosclerotic narrowings in all patients. During pacing, 16 patients developed anginal pain, and their LVEDP increased significantly. The other 18 patients had no angina and no significant change in LVEDP. In these 18 patients, there were no significant changes throughout the pacing study in myocardial balances of lactate, glucose, potassium, and inorganic phosphate. In contrast, the 16 patients with induced angina during pacing showed a significant myocardial production of lactate and a loss of potassium. Myocardial inorganic phosphate loss was not statistically significant. There was no significant change in myocardial glucose extraction during angina, although a slight increase was observed during the 1st min afer pacingmthere was no correlation between the arterial concentration and the myocardial extraction of these substances. N stoichiometric relationship was found between glucose and lactate or between potassium and inorganic phospahte balance; Myocardial extraction and production of lactate correlated best with inorganic phosphate uptake and loss. In the preset study, lactate was a more reliable metabolic indicator of myocardial ischemia than potassium and inorganic phosphate, although these last two substances may be helpful in acheiving a greater accuracy for biochemical diagnosis of ischemia. Myocardial glucose balance was of no value as a metabolic indicator of ischemia in this pacing study.

To determine whether women with mitral valve prostheses can improve their physical fitness without suffering cardiac dysfunction or hemolysis, 10 women (mean age 47 years) who had undergone mitral valve replacement (an average of 3.7 years earlier) were enrolled in an 8-week program of exercise on a bicycle ergometer. They exercised three times a week, starting at 60% and increasing to 80% of their maximal heart rate achieved during stress testing. Nine other women with similar clinical characteristics (mean age 48 years) constituted a control group. Exercise produced significant cardiovascular improvement, as evidenced by a mean decrease of 12 beats/min in the heart rate at steady-state work load (p less than or equal to 0.01), a mean increase of 121 kpm in the maximal tolerated work load (p less than or equal to 0.01), and a mean increase of 4 ml/kg X min-1 in the peak oxygen consumption (p less than or equal to 0.01). There was a small increase in the mean plasma hemoglobin level (15 to 29 mg/dl) and the mean reticulocyte count (1.8% to 2.4%) after the program (p less than or equal to 0.05). There were no significant changes in any of the variables studied in the control group. There were no changes in the clinical, electrocardiographic or echocardiographic findings in the experimental group. Although slightly increased hemolysis may occur, women with mitral valve replacement can improve their cardiovascular condition by exercising.

Causal blood pressure measurements were recorded in two groups of men aged 40 to 64 years; of the 7024 men in metropolitan Saint John, NB, and the 4044 men in seven suburbs of Quebec who were asked, 5840 (83.1%) and 3097 (76.6%) respectively agreed to participate. Of the Saint John group 9.0% were taking antihypertensive drugs, as compared with only 3.3% of the Quebec group (p less than 0.0001). Among the treated subjects 33% in Saint John and 53% in Quebec still had a diastolic pressure greater than 95 mm Hg (p less than 0.01). Among the participants not taking antihypertensive drugs the systolic blood pressure increased with age, but the diastolic blood pressure increased only slightly up to 55 years of age and then decreased. On average the subjects in Saint John who were not being treated had a systolic pressure 6.2 mm Hg lower and a diastolic blood pressure 3.6 mm Hg lower than their Quebec counterparts (p less than 0.0001). This difference was observed in all the age groups and was not the result of the treatment of a greater proportion of the Saint John cohort. Despite the higher blood pressures and the smaller number receiving adequate treatment in the Quebec group, the rate of death due to coronary artery disease was 10% lower than that in the Saint John group. A bias in the data from Quebec may have influenced the magnitude of the differences between the two samples, but if present it should have underestimated the blood pressures in the Quebec group and therefore not have changed the outcome.

To determine whether cardiac interstitial spaces participate in cardiac fatty acid pool, the relationship between cardiac lymph and arterial plasma free palmitate and triglycerides was studied in anesthetized dogs [14C]Sucrose, infused at a constant rate in a femoral vein, appeared in the lymph at 90% of its arterial concentration within 60 min. On the other hand, when [1-14C]palmitate was infused at the same rate and at the same site, the ratio of lymph to arterial plasma 14C-labelled free fatty acids (FFA) was only 21% at 60 min and 25% at 120 min, even though the concentrations of endogenous FFA in lymph and arterial plasma were the same. The ratio reached 90% only 24 h after a bolus injection of [3H]palmitate. [1-14C]Palmitate in the lymph triglyceride fraction was only 8% of that in plasma. Although the lymph composition may be influenced by the metabolism of heart muscle, cardiac adipose tissue, and serum lipoproteins, these results indicate the presence of a pool of myocardial fatty acids which may be partly located in the interstitial spaces.

Improved prosthetic aortic valves have reduced the incidence of complications to a point where it can be hypothesized that functional class I subjects after aortic valve replacement (AVR) should adapt to a vigorous training program without a significant increase of hemolytic activity or clinical signs of prosthesis malfunction. To test this hypothesis, 10 men (mean age 52 years) who had undergone AVR (7 Björk-Shiley and 3 Lillehei-Kaster) were submitted to an 8-week training program on ergometer, 3 times/week, from 60 to 80% of individual maximal heart rate. Ten other men who had undergone AVR but did not participate in the training program were control subjects. The exercise program produced significant improvements in posttraining maximum tolerated ergometer work load (210 kpm, p less than 0.001), in maximum total body oxygen consumption (5 ml/kg X min-1, p less than or equal to 0.01) and in double product at submaximal work load (-5,126, p less than or equal to 0.01). After training, hemoglobin decreased by about 1 g% (p less than or equal to 0.05) and hematocrit, reticulocyte counts and haptoglobin did not change significantly. Serum LDH and serum AST did not increase. Pre- and post-training echocardiograms did not show detectable alterations. Thus, patients with AVR who are in functional class I can adapt to a physical exercise program without significant adverse effects.

In patients with a strongly positive exercise electro-cardiogram, the workload achieved during the test allows the identification of subsets with good or poor survival rates. To determine whether the same criteria also predict acute ischemic heart events such as unstable angina and myocardial infarction, fatal and nonfatal acute manifestations were documented in 241 patients medically treated during an 8-year follow-up. All patients had a Bruce protocol treadmill exercise test with ST-segment depression greater than or equal to 2 mm and coronary angiographic studies. There were 52 deaths; of these 44 were due to coronary artery disease. There were 41 episodes of unstable angina and 21 myocardial infarcts documented as first morbid events. As expected, survival improved with increased workload achieved; patients terminating their exercise at stage I (5.1 METs) had an 8-year survival rate of 45 +/- 9% while those reaching stage IV or more (10 METs) had a survival rate of 93 +/- 6%. In a multivariate analysis, the duration of exercise and the number of narrowed coronary arteries and of left ventricular segment abnormalities correlated significantly with survival. In contrast, nonfatal acute events occurred in about 20 to 35% of patients whatever the stage of the exercise test. Furthermore, neither variables during the exercise test nor angiographic findings predicted nonfatal events. Thus, although the workload achieved did identify patients with different mortality rates, it failed to predict subsets of patients with different morbid event rates.

The value of myocardial scanning with 43K was assessed in 64 consecutive patients undergoing coronary arteriography, and in five young volunteers. Myocardial scans at rest detected only 16 of the 35 transmural infarcts documented on electrocardiograms, 11 of 11 anterior infarcts and five of 24 in other sites. Myocardial scans were obtained immediately after a graded exercise test in the five normal volunteers, in nine patients with normal coronary arteriograms and in 25 patients with atherosclerotic narrowing greater than 75% involving the left anterior descending artery, with or without disease of other coronary vessels. All patients with normal coronary arteriograms had normal myocardial scans. A regional perfusion deficit was observed after exercise in all six patients with single vessel disease, but in only 11 of the 19 patients with disease involving two or three vessels. Although the technique was specific, it lacked sensitivity, due mostly to poor resolution and the location of the disease.

The objectives of this study were to determine the incidence of high blood pressure (HBP) in Quebec suburbs and evaluate age, baseline blood pressure level and overweight as determinants of future hypertension. From a cohort of 4828 men, aged 35-64, screened in 1974, 1090 normotensives (blood pressure less than 160/95 mmHg without medication) free of cardiovascular disease were re-evaluated in 1979-1980. Among these 1090 men, 183 have developed a blood pressure greater than or equal to 160/95 mmHg or less than 160/95 mmHg associated with antihypertensive medication. There was no significant variation of the incidence by age (10-year strata). In the group of subjects with a baseline systolic blood pressure (SBP) between 140 and 159 mmHg the incidence of systolic hypertension was 6.3 times higher than in the group with baseline SBP less than 140 mmHg. Similarly, in the group of subjects with a baseline diastolic blood pressure (DBP) between 90 and 94 mmHg the incidence of diastolic hypertension was 3 times higher than in the group with a baseline DBP less than 90 mmHg. The incidence of HBP was correlated with overweight. Furthermore overweight was a highly prevalent risk factor in the study population. In summary, the incidence of HBP is 169 per 1000 in 5 years. Baseline blood pressure and overweight are strong determinants of a future HBP and can be used to identify the high risk subgroup.

To determine whether beta blockers prevent the more rapid onset of effort angina during the postprandial state, metoprolol 100 mg was given before and after an 800-calorie meal in 12 male patients with stable angina and coronary artery disease. Three graded treadmill exercise tests were done daily on 2 days. After an overnight fast the first test on each day was done after a placebo to detect day-to-day variations. The second test was done 90 min after metoprolol or placebo given orally in a double-blind randomized fashion. Immediately thereafter the patients ate their meal and did their third test 30 min later. There was no significant difference between the first test on each day. After placebo the postprandial state was associated with an earlier onset of effort angina (310 and 370 sec, p less than 0.01) and with greater heart rate and systolic blood pressure rises for any work load. After metoprolol, however, there was no significant difference between the pre- and postprandial findings. During the postprandial state metoprolol delayed the onset of angina more than placebo (385 and 310 sec) and positive electrocardiogram (310 and 228 sec) and induced lowering of maximal heart rate (120 and 144 bpm) and systolic blood pressure (157 and 187 mm Hg) (p less than 0.01). Metoprolol slowed the rapid onset of effort agina during the postprandial state.

The lipid profiles of 1165 French Canadian men (aged 42 to 59 years) were studied and related to drinking and smoking habits. Alcohol consumption and smoking were closely related, smokers consuming twice as much alcohol as non-smokers. When relative body weight, total cholesterol, triglyceride and alcohol consumption were controlled in a covariate analysis, plasma levels of high density lipoprotein (HDL) cholesterol, HDL2 and HDL3 differed significantly between smokers, ex-smokers and nonsmokers. Ex-smokers had higher levels of HDL cholesterol than nonsmokers who had higher levels than smokers. The higher levels of HDL in ex-smokers could be explained by the confounding effects of alcohol intake. Alcohol users had significantly higher levels of HDL cholesterol, HDL2 and HDL3 than nondrinkers. Men who drank the equivalent of more than 3 ounces of absolute alcohol per week had significantly higher levels of HDL cholesterol and HDL3 than those who drank less than 3 ounces or did not drink at all. HDL2 levels were only significantly different between nondrinkers and those who consumed more than 3 ounces per week. These results show that smoking and alcohol have strong but opposing effects on HDL and its subfractions in middle-aged French Canadian men.

To determine the prognosis of patients with painless strongly positive exercise electrocardiogram, the 6-year cumulative survival rate was computed for 298 medically treated patients who terminated their exercise test with or without angina. All had horizontal or downsloping ST depression greater than or equal to 2 mm during a treadmill exercise test according to the standardized multistage Bruce protocol. Of the 298 patients, 119 terminated the exercise test because of dyspnea or fatigue and 179 stopped because of angina. Among the 119 patients without angina, there were 18 deaths, 16 from coronary artery disease (CAD), of which 8 occurred suddenly. Among the 179 patients with exercise-induced angina, 36 died, 33 from CAD, of which 13 were sudden deaths. The overall 6-year survival rate was 85 +/- 3% for patients without angina and 80 +/- 3% in those with angina (p less than 0.05). However, patients without angina achieved a significantly longer duration of exercise and had higher maximal heart rate and systolic blood pressure during exercise. In both groups, survival decreased with decreasing duration of exercise. In patients without angina, the 6-year survival rate was 97 +/- 3% in those achieving stage IV (greater than or equal to 541 s), 87 +/- 4% in stage III (361 to 540 s), 64 +/- 13% in stage II (181 to 360 s) and 60 +/- 15% in stage I (less than or equal to 180 s).(ABSTRACT TRUNCATED AT 250 WORDS)

To determine the effect of perfluorocarbon (PFC) hemodilution on myocardial vessel capacity to autoregulate, circumflex coronary artery pressure-flow relations were studied in anesthetized dogs under three conditions: maximal vasodilatation before and after PFC; autoregulation before and after PFC with 100% oxygen supplemented with room air ventilation, and autoregulation with PFC hemodilution during either room air or 100% oxygen supplemented with room air ventilation. During coronary vasodilatation, PFC did not modify coronary conductance or zero-flow pressure. During autoregulation after PFC, the lower pressure limit of the autoregulatory pressure-flow relation was shifted leftward. This leftward shift occurred because endocardial blood flow was maintained at a lower coronary perfusion pressure with PFC while epicardial blood flow was unchanged. Endocardial blood flow was also preserved at 50% of control blood flow levels as evidenced by the higher endocardial-epicardial blood flow ratio with PFC. After PFC with 100% oxygen supplemented with room air ventilation, oxygen transport increased significantly when coronary perfusion pressure was below the lower pressure limit; the effect was most prominent in the endocardial tissue layer. Thus, PFC shifts the lower pressure limit to the left because of the increased ability of the endocardial vessel to autoregulate. Consequently, PFC can be considered a useful intervention for improving endocardial oxygen transport at low coronary perfusion pressures.

The potential antianginal effects of orally administered ethyl-adenosine-5-carboxylate hydrochloride (EACH) were assessed in 9 patients with stable angina pectoris who underwent two standardized exercise tests for 3 consecutive days. The first daily exercise performed after placebo revealed no daily variation. The second test was preceded by placebo, 26 mg EACH or 33 mg EACH administered in a double-blind fashion with the use of crossover design. After the completion of the study in the first 6 patients, the 33-mg dose of EACH had to be discontinued because 3 patients had severe angina and another one had nausea and diffuse numbness after this dose. In the remaining 3 patients a 6-mg dose of EACH was used instead of 33 mg, after which the study was terminated because no difference could be determined. EACH, 26-mg and 6-mg, had no significant effect on resting and exercise heart rate, on blood pressure, on onset or duration of angina and positive-exercise electrocardiogram, or on exercise duration. Our study revealed that EACH had no potential antianginal effect and that at a dosage of 33 mg it may induce angina.

In 34 patients with coronary atherosclerosis a pacing test was performed with measurement of the lactate, glucose, potassium and inorganic phosphate coronary arterio-venous differences. Eighteen of these 34 patients felt no pain during the pacing test. In this group of asymptomatic patients, there was no significant change of the lactate, glucose, potassium and inorganic phosphate myocardial extraction. In the 16 patients who felt an anginal pain during the pacing test, there was a significant myocardial production of lactate, but the myocardial loss of potassium and inorganic phosphate was not continuously statistically significant. Myocardial extraction of glucose during the pacing-induced angina did not increase. Although, in some patients, both the potassium and the inorganic phosphate might be used to assess a condition of myocardial ischaemia, the lactate remains the best metabolic criterion for pacing-induced ischaemia.

The objects of these experiments were to determine to what extent oleic acid, removed from plasma by forearm muscles, was oxidized immediately, and to search for evidence of an intramuscular lipid pool which may be composed to triglycerides synthesized from plasma free fatty acids and which may supply substantial portions of lipid substrates for oxidation by muscle. To these ends (1-14C]oleic acid was infused at constant rate into the brachial artery of seven healthy young men at rest in the postabsorptive state. Results were: (1) muscle respiratory quotient (0.76) implied that about 80% of the oxygen consumed was for the oxidation of lipid. (2) Muscle free fatty acid uptake, had it been oxidized directly, could account for more than 100% of observed oxygen uptake. (3) There was a lag of at least 30 min before 14CO2 appeared in forearm venous blood. (4) 14CO2 release from forearm muscle tended to reach an apparent plateau after 3 h of infusion of [14C]oleic acid. (5) During the time of plateau 14CO2 release, oleic acid extracted from plasma could account for only 20% of oxygen consumption; most of the oleic acid taken up was not oxidized directly. (6) 14CO2 release persisted at a high level during the 1-3 h follow-up period after the infusion ended. (7) Neither the delay in initial appearance of 14CO2 nor its continued release after cessation of infusion was due to delay and distribution in a forearm CO2 pool, since intra-arterial infusion of NaH14CO3 in additional subjects demonstrated much more rapid distribution of 14CO2 in the forearm. Results show that most, if not all, free fatty acids taken up by resting muscle are not oxidized directly, but probably enter an intramuscular pool which has a slow turnover during resting metabolism and is the immediate source of oxidized lipid substrate.

To investigate the mechanism by which muscular coronary overbridging can cause myocardial ischaemia, we studied the effect of systolic compression (SC) of the proximal left circumflex coronary artery in ten anaesthetised dogs, with both intact autoregulation and maximally dilated coronary arteries. Systolic compression was produced by a mechanical device adjusted to interrupt circumflex coronary flow only during the aortic ejection period and we measured left ventricular, aortic and distal circumflex coronary pressures, phasic coronary blood flow, regional myocardial blood flow (RMBF), myocardial oxygen consumption (MVO2), and myocardial lactate extraction (MLE). During both autoregulation and maximal coronary vasodilatation, there was a diastolic time lag after SC to restart phasic circumflex coronary blood flow (34 +/- 3 vs 31 +/- 3 ms) and to increase distal circumflex coronary pressure (69 +/- 4 vs 79 +/- 6 ms). With autoregulation, SC reduced the diastolic circumflex coronary: systolic left ventricular pressure time ratio (DPTIc:SPTI) and there were no changes in the other measured variables. During maximal coronary vasodilatation and SC, the coronary vasodilator reserve, the DPTIc:SPTI ratio and the inner:outer myocardial blood flow distribution were decreased in the territory of the left circumflex coronary artery; a linear relationship was observed between the DPTIc:SPTI and the inner:outer myocardial blood flow ratio. Systolic compression during vasodilatation also produced a reduction in myocardial oxygen consumption of the whole heart and a production of lactate in the coronary sinus. These results suggest that myocardial ischaemia with a myocardial bridge is due to the combined effects of a diastolic time lag to repressurise the coronary vascular bed, of tachycardia and of coronary vasodilatation.

To evaluate whether elevated arterial free fatty acids (FFA) increase myocardial oxygen demand and ischemia, 15 fasting patients with coronary artery disease underwent a standardized atrial pacing test before (PTI) and during (PT2) heparin infusion. The patients were monitored for clinical and electrocardiographic (ECG) manifestations of ischemia. Myocardial extraction of lactate, inorganic phosphate, oxygen and FFA was measured before and during each PT. The control arterial FFA was 0.65 +/- 0.03 micromole/ml and rose to 1.83 +/- 0.16 micromole/ml during heparin influsion. Myocardial oxygen extraction at rest and during PT was not affected by the increase in arterial FFA. Seven patients asymptomatic during PT1 did not develop ischaemic manifestations during PT2. In eight patients with angina during both PTs, increased arterial FFA concentration did not modify the severity of anginal pain, the amount of ST-segment depression and the myocardial balance of lactate or inorganic phosphate. Elevation of arterial FFA by heparin neither increased myocardial oxygen extraction at rest or during pacing nor accentuated ischemic manifestations during PT.

There is evidence that patients with signs of poor left ventricular function or marked ischemia at low work load during an exercise test have a poor prognosis for survival. To determine whether a pacing test can provide similar information, the 6-yr survival rate was computed in 118 medically-treated patients who had undergone a standardized atrial pacing test. Among the 118 patients, 80 had significant coronary artery disease (CAD). The variables measured for the atrial pacing test were: induced angina, myocardial lactate extraction (MLE), maximal heart rate (MHR) and left ventricular end-diastolic pressure (LVEDP) changes. There was no death in 38 patients without significant CAD. The 6-yr survival rate of the 80 patients with CAD was 84 +/- 4% (+/- SEM). Of all the variables, the combinations of MHR less than or equal to 150 beats min-1 during pacing associated with a LVEDP increase greater than or equal to 5 mmHg immediately after pacing or with MLE less than or equal to 0% during pacing constituted the best predictors. Patients with a MHR less than or equal to 150 beats min-1 and a LVEDP increase greater than or equal to 5 mmHg had a 6-yr survival of 56 +/- 12% in comparison to 92 +/- 3% for the remaining patients (P less than 0.001). Patients with a MHR less than or equal to 150 beats min-1 and MLE less than or equal to 0% during pacing had a 6-yr survival of 64 +/- 11% in comparison to 91 +/- 4% for the remaining patients (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Plasma lipid and lipoprotein levels were determined in a randomly selected population of 1169 French-Canadian men in the Quebec City area. The mean levels of total plasma cholesterol and triglycerides were 224.0 and 166.5 mg/dL respectively. The mean level of low-density lipoprotein cholesterol was higher and the mean level of high-density lipoprotein (HDL) cholesterol lower than those reported in a recent study in English-Canadian men. The mean HDL2 and HDL3 levels were lower than those reported in American men. Stratification of plasma triglyceride levels for all age groups showed that mean HDL2 levels decreased rapidly with moderate rises in triglyceride levels. Less than 9% of the variation in lipid or lipoprotein levels was related to age or relative body weight. Education had no significant effect on the levels.