Effect of endurance exercise training on heart rate variability at rest in healthy young and older men.

Heart rate variability (HRV) (SD of the RR interval), an index of parasympathetic tone, was measured at rest and during exercise in 13 healthy older men (age 60 to 82 years) and 11 healthy young men (age 24 to 32 years) before and after 6 months of aerobic exercise training. Before exercise training, the older subjects had a 47% lower HRV at rest compared with the young subjects (31 +/- 5 ms vs 58 +/- 4 ms, p = 0.0002). During peak exercise, the older subjects had less parasympathetic withdrawal than the young subjects (-45% vs -84%, p = 0.0001). Six months of intensive aerobic exercise training increased maximum oxygen consumption by 21% in the older group and 17% in the young group (analysis of variance: overall training effect, p = 0.0001; training effect in young vs old, p = NS). Training decreased the heart rate at rest in both the older (-9 beats/min) and the young groups (-5 beats/min, before vs after, p = 0.0001). Exercise training increased HRV at rest (p = 0.009) by 68% in the older subjects (31 +/- 5 ms to 52 +/- 8 ms) and by 17% in the young subjects (58 +/- 4 ms to 68 +/- 6 ms). Exercise training increases parasympathetic tone at rest in both the healthy older and young men, which may contribute to the reduction in mortality associated with regular exercise.

Variability of digitized left ventricular M-mode echocardiography: a study in healthy subjects and patients with repaired tetralogy of Fallot.

To assess possible factors affecting the variability of digitized left ventricular M-mode echocardiograms, the influence of respiration and the variability due to different beats and observers were analysed in 11 healthy subjects and 11 patients with repaired tetralogy of Fallot. Left ventricular end-diastolic dimension (LVEDD) decreased from end-expiration to end-inspiration in the healthy subjects, but not in the patients. The maximal rate of dimension change decreased in both healthy subjects and patients from end-expiration to end-inspiration. The beat-to-beat variability assessed by the coefficient of variation (CV,%) between measurements of one cardiac cycle was twice the CV for three cycles, whereas the CV for three and five cardiac cycles was not different. The CV for intraobserver variability was less than 5.0% for dimensions and less than 13.0% for the rates of dimension change, whereas the interobserver variability had CV of 17.1% for rates of dimension changes. The influence of respiration and different observers on the variability of LV end-systolic dimension and shortening fraction was larger in the patients than in the healthy subjects. Thus, to obtain optimal technique for analysis of digitized LV M-mode echocardiograms in serial patient studies, the number of observers should be kept at a minimum and at least 3 beats at end-expiration should be used.

[Angina pectoris after coronary angioplasty. Restenosis or partial revascularization]. / Angina pectoris etter koronar angioplastikk. Restenose eller unfullstendig revaskularisering.

Percutaneous transluminal coronary angioplasty (PTCA) was performed on 115 consecutive patients with angina pectoris and the results were evaluated after an average of 100 days by means of bicycle exercise test and coronary angiography. Complete revascularization was achieved in 75% of the patients. Restenosis occurred in 23%. A good symptomatic effect was found in 90% of the patients with complete revascularization and in 72% of the patients with partial revascularization. Recurrence of angina pectoris 4-8 weeks after PTCA is a predictor of restenosis. Absence of angina and a negative bicycle exercise test 3-4 months after PTCA are strong predictors of the absence of restenosis.

Left ventricular function in myasthenia gravis.

Myasthenia gravis is an autoimmune disorder with autoantibodies to acetylcholine receptors of skeletal muscle. Left ventricular diastolic function was studied with M-mode and Doppler echocardiography in 25 patients with myasthenia and in a group of age- and heart rate-matched control subjects. In the patients, diastolic peak filling rate was reduced by 37%, and Doppler peak early filling velocity (E) was reduced by 12% compared with the control subjects (2.7 +/- 0.7 vs 4.2 +/- 1.0 s-1, and 76 +/- 8 vs 85 +/- 15 cm/s, respectively; p less than 0.05). Peak atrial filling velocity (A) was increased by 38% (68 +/- 17 vs 48 +/- 9 cm/s; p less than 0.01), and consequently the E:A ratio in the group of patients was reduced by 33% (1.22 +/- 0.40 vs 1.81 +/- 0.33; p less than 0.001). End-diastolic dimension was 5.0 +/- 0.5 cm in both groups, heart rate was 70 +/- 12 vs 68 +/- 16 beats/min (p = not significant [NS]), M-mode ejection fraction was 76 +/- 8 vs 79 +/- 5% (p = NS), M-mode peak ejection rate was -1.9 +/- 0.4 vs -2.1 +/- 0.3 s-1 (p = NS), and peak aortic outflow velocity was 109 +/- 18 vs 98 +/- 13 cm/s (p = NS). Twenty-three patients and 15 control subjects were studied before and after intake of the acetylcholine-esterase inhibitor pyridostigmine.(ABSTRACT TRUNCATED AT 250 WORDS)

The relation between radionuclide angiography and Doppler echocardiography during contractile changes with infusions of epinephrine.

To define the quantitative relations between radionuclide and Doppler measures of systole during sympathetic activation with epinephrine, 10 young normal men were studied with simultaneous radionuclide angiography and M-mode and Doppler echocardiography during graded infusions of epinephrine (10, 25 and 50 ng/kg/min for 12 minutes each). During a nine-fold increase in circulating levels of epinephrine in arterialized plasma (94 +/- 59 to 879 +/- 310 pg/ml, P less than 0.001), the heart rate increased from 58 +/- 8 to 73 +/- 7 beats/min (P less than 0.01), whereas the mean arterial pressure fell from 82 +/- 3 to 75 +/- 6 mmHg (NS) and end-systolic wall stress decreased from 97 +/- 6 to 67 +/- 10 dynes/sec (P less than 0.01). The ejection fraction as estimated using radionuclide techniques increased from 68 +/- 6 to 83 +/- 6%, the peak ejection rate measured in this way increased from -3.36 +/- 0.3 to -5.10 +/- 0.5 end-diastolic volumes/sec, the ejection fraction as estimated with M-mode echocardiography increased from 66 +/- 5 to 83 +/- 5%, the echocardiographic ventricular dimension shortening increased from -1.78 +/- 0.2 to -2.7 +/- 0.4 sec-1, the peak aortic outflow velocity as measured with Doppler techniques increased from 98 +/- 13 to 147 +/- 25 cm/sec, and the aortic outflow acceleration velocity increased from 11 +/- 3 to 27 +/- 7 m/sec2 (all P less than 0.001). There was a significant correlation between the changes in radionuclide and M-mode estimations of ejection fractions (r = 0.82), between the radionuclide peak ejection rate and M-mode peak dimension shortening (r = 0.80) and between the radionuclide peak ejection rate and the Doppler peak aortic outflow velocity (r = 0.90) (all P less than 0.01). We conclude that corresponding radionuclide and Doppler echocardiographic measurements of systolic function are altered similarly during increased sympathetic activation with epinephrine.

Influence of sympathetic stimulation and parasympathetic withdrawal on Doppler echocardiographic left ventricular diastolic filling velocities in young normal subjects.

To determine the effects of parasympathetic withdrawal or sympathetic stimulation on Doppler echocardiographic measures of left ventricular diastolic filling, we studied 10 young normal subjects aged 21 to 29 years during separate infusions of atropine (0.8 mg followed by 0.4 mg every 10 minutes until heart rate greater than 110 beats/min or a total dose of 2 mg was attained) and epinephrine (10, 25 and 50 ng/kg/min for 12 minutes each). At the highest atropine dose, heart rate increased from 60 +/- 9 to 105 +/- 8 beats/min (mean +/- standard deviation), the diastolic filling period decreased by 61% (573 +/- 141 to 222 +/- 34 ms), the peak early (E) filling decreased 23% (77 +/- 12 to 61 +/- 11 cm/s), the peak atrial (A) filling increased 103% (40 +/- 6 to 81 +/- 17 cm/s), and the E/A ratio decreased by 60% (2.0 +/- 0.5 to 0.8 +/- 0.3) (all p less than 0.001). These alterations were not correlated to changes in systolic function, preload, blood pressure or plasma catecholamines, all of which were unchanged. However, atropine-induced changes in diastolic filling period were highly correlated to changes in E peak (r = 0.64, p less than 0.01), A peak (r = -0.95, p less than 0.001) and the E/A ratio (r = 0.93, p less than 0.001). The effects of atropine on the E/A ratio were normalized by dividing the E/A ratio by the diastolic filling period (E/A/diastolic filling period).(ABSTRACT TRUNCATED AT 250 WORDS)

[The usefulness of thallium-201 scintigraphy in the diagnosis of coronary disease]. / Nytten av 201-thalliumscintigrafi i diagnostisering av koronarsykdom.

Stress thallium scintigraphy was performed in 60 patients with chest pain of uncertain origin. Myocardial ischemia was identified in 91% of the 47 patients who had angiographically significant coronary artery stenoses. Sensitivity of thallium scintigraphy was highest in patients with stenosis in the left descending coronary artery (LAD); 91% of the patients had abnormal thallium as compared with 67% of the patients with normal LAD but significant stenoses in the circumflex artery and/or the right coronary artery. Perfusion defects in the circumflex in only 50% of the patients with multiple vessel disease. We conclude that stress thallium scintigraphy is a useful diagnostic procedure in patients with chest pain of uncertain origin and identifies the patients to be selected for coronary artery angiography.

Influence of myocardial infarction size on radionuclide and Doppler echocardiographic measurements of diastolic function.

To assess the relation between myocardial infarction size and diastolic function as measured by radionuclide ventriculography and Doppler echocardiography, 83 patients (aged 58 +/- 9 years) without significant valvular disease were studied 8 to 12 weeks after an acute myocardial infarction. Myocardial infarction size was measured by resting thallium-201 tomography. Peak early filling rate (in end-diastolic volumes/s) was measured by gated blood pool scintigraphy. Doppler measures of mitral inflow were peak early (E) and atrial (A) filling velocities, slopes of E and A, percent E and A filling, E/A ratio and diastolic filling period. In univariate analyses, there was a significant inverse correlation between infarction size and the peak early filling rate (r = -0.59, p less than 0.001), and this remained significant (r = -0.63, p less than 0.0001) in an analysis that included 2 other determinants of the filling rate, age and diastolic filling period. Infarction size was directly correlated to the peak E velocity (r = 0.37, p less than 0.01), deceleration of E (r = 0.41, p less than 0.01) and percent E filling (r = 0.31, p less than 0.01), and was inversely correlated to peak A (r = -0.27, p less than 0.05) and percent A filling (r = -0.26, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Echocardiographic evaluation of segmental wall motion early and late after thrombolytic therapy in acute myocardial infarction: the Western Washington Tissue Plasminogen Activator Emergency Room Trial.

In 92 acute myocardial infarction (AMI) patients treated with tissue plasminogen activator 2.3 +/- 1.2 hours after the onset of chest pain, echocardiography was performed at 11 +/- 14 hours (early) and, in 49 patients, again at 13 +/- 7 weeks (late). Infarct location and the left ventricular wall motion score index--the average score (normal = 1, hypokinetic = 2, akinetic = 3, dyskinetic = 4) for 20 segments--were determined by 2 observers unaware of clinical, angiographic or electrocardiographic data. Concordance between noninvasive infarct location by electrocardiography or echocardiography and infarct-related artery at angiography 4 +/- 2 days later (n = 85) was 76 and 81%, respectively. The early wall motion score index was worse for anterior (1.8 +/- 0.4) versus inferior (1.3 +/- 0.2, p less than 0.0001) or posterior-lateral (1.6 +/- 0.2, p = 0.0003) infarcts. Overall, the wall motion score index improved from early to late echocardiography (n = 49, 1.5 +/- 0.3 to 1.3 +/- 0.3, p = 0.0008). However, improvement was confined to those with time to treatment less than or equal to 2 hours (n = 22, 1.4 +/- 0.3 to 1.2 +/- 0.2, p less than 0.0001), and evidence of reperfusion at angiography (n = 38, 1.5 +/- 0.3 to 1.2 +/- 0.3, p less than 0.0001). The decrease in the wall motion score index was related to a decrease in the number of adjacent involved segments (5.5 +/- 3.0 to 3.7 +/- 3.9/patient, p = 0.0006). Thus, echocardiography early after AMI identifies infarct location. Improvement in regional wall motion is seen after early treatment with intravenous tissue plasminogen activator.

Fate of left ventricular thrombi in patients with remote myocardial infarction or idiopathic cardiomyopathy.

Although left ventricular thrombi that form acutely after myocardial infarction frequently resolve spontaneously or with anticoagulant therapy, the fate of left ventricular thrombi in patients with remote myocardial infarction or with idiopathic cardiomyopathy remains unknown. To determine the natural history of such chronic left ventricular thrombi, we performed serial echocardiograms on 51 patients with remote myocardial infarction (greater than or equal to 3 months; mean, 31 +/- 41 months) and on nine patients with idiopathic dilated cardiomyopathy. Mean follow-up was 24 +/- 22 months during which 3.5 +/- 1.4 echocardiograms were obtained. Studies were interpreted by blinded observers, and an increase or decrease of more than 5 mm in maximal thrombus thickness was defined as significant. Among all 60 patients left ventricular thrombi were unchanged in 24 (40%), completely resolved in 24 (40%), decreased in size in four (7%), increased in size in five (8%), and decreased and then increased in size in three (5%). Results in patients with remote infarction and idiopathic cardiomyopathy were similar. Warfarin therapy, which was at the discretion of the primary physician, was associated with a higher prevalence of thrombus resolution compared with no therapy (59% vs. 29%, p = 0.02). Definite systemic emboli occurred in seven patients (12%), all at times while they were not anticoagulated. Among the 48 thrombi that were present on two or more echocardiograms, changes in thrombus shape (classified as protruding or flat) occurred in only 16%, and changes in thrombus movement (classified as mobile or immobile) occurred in only 10%.(ABSTRACT TRUNCATED AT 250 WORDS)

Risk factors for embolisation in patients with left ventricular thrombi and acute myocardial infarction.

Risk factors for systemic embolisation in patients with ventricular thrombi caused by an acute myocardial infarction were studied in 150 consecutive patients with an infarction of the anterior wall. Serial echocardiograms were performed 2-10 days after the acute event and patients were followed up for three months. Anticoagulation treatment was started only after the detection of thrombi. Of the 55 patients in whom a thrombus developed, 15 (27%) had peripheral emboli between 6-62 days; but only two (2%) of 95 patients without thrombus had emboli. Among 15 variables, the best single predictors of embolisation were age greater than 68 years (80% sensitive, 85% specific), pendulous thrombus (60%, 93%), and independent thrombus mobility (60%, 85%). Logistic regression analysis showed that a formula that included patient age, thrombus area, and the length of thrombus in the ventricular lumen predicted embolisation (sensitivity 87%, specificity 88%). There was no correlation between age and the thrombus variables. The risk of embolisation from left ventricular thrombi in acute anterior myocardial infarction can be accurately assessed from patient age and echocardiographic features. The risk of peripheral emboli is high in patients with left ventricular thrombi and those aged greater than 68.

Left ventricular thrombi after short-term high-dose anticoagulants in acute myocardial infarction.

To examine the effect of short-term, high-dose anticoagulation on the subsequent occurrence of left ventricular (LV) thrombi after a first anterior wall acute myocardial infarction (AMI), 21 patients received placebo and 21 high-dose anticoagulants during the first 10 days of the acute infarction. They were studied with cross-sectional echocardiography 10 days and 1.3 and 6 months post infarction. At 1 month, 6 of 7 thrombi present in the placebo group at 10 days were still visible. No thrombi were detected at 10 days in the anticoagulation group, but 6 patients had developed a LV thrombus at 1 month. These 12 patients with LV thrombi were subsequently treated with oral warfarin for 2 months, after which all thrombi had disappeared. Warfarin was then discontinued, and a thrombus had recurred in 5 patients after 6 months. Apical akinesis at 10 days was a predictor for thrombus with a sensitivity and specificity of 100% and 72.2%, respectively. Three of the 13 patients with LV thrombi suffered stroke in contrast to none without thrombi (P = 0.025). We conclude that after discontinuation of short-term high-dose anticoagulation therapy in anterior AMI, LV thrombi may develop rapidly and lead to embolic complications, particularly in patients with persisting apical akinesis.

Peripheral emboli from left ventricular thrombi of different echocardiographic appearance in acute myocardial infarction.

In four patients with anterior wall acute myocardial infarction (AMI) and left ventricular thrombi diagnosed by two-dimensional (2-D) echocardiography, disappearance of left ventricular thrombi was demonstrated by 2-D echocardiography immediately after the patients had suffered peripheral emboli. Two thrombi were pendulous with free motion during the cardiac contractions; one of these consisted of two separated pendulous clots that disappeared after two episodes of embolization six and 16 days, respectively, after the onset of AMI. Two thrombi were initially broad based, flat, and without intracavitary motion. One thrombus caused two episodes of peripheral emboli; the other began as a flat thrombus without intracavitary motion but progressed to show central echolucency and, then, vigorous intracavitary motion of the margin prior to embolization. Five of six embolic episodes occurred when these patients were receiving high-dose anticoagulants. These anticoagulants were administered once the thrombi were diagnosed. Left ventricular thrombi of very different appearance on 2-D echocardiography may cause embolization, which may occur during therapeutic anticoagulation administered after thrombi have developed in patients with AMI.

Increased occurrence of left ventricular thrombi during early treatment with timolol in patients with acute myocardial infarction.

To examine whether early intervention with timolol influences the occurrence of left ventricular thrombi in acute anterior myocardial infarction, 40 patients with acute anterior myocardial infarction admitted to hospital within 6 hr of onset of symptoms were randomly assigned to receive intravenous followed by oral timolol maleate or placebo. Five (25%) of 20 patients in the placebo group and 14 (73.7%) of 19 patients with confirmed infarction in the timolol group developed a left ventricular apical thrombus as detected by two-dimensional echocardiography from 2 to 10 days after inclusion (p less than .005). Patients received anticoagulants only after a left ventricular thrombus had been diagnosed. Only one patient with thrombus suffered peripheral embolization (timolol group). The treatment groups were comparable with respect to location of regional left ventricular dysfunction, electrocardiographic changes, and infarct size estimated by creatine kinase release. However, computer-assisted regional wall motion analysis demonstrated significantly reduced apical wall motion in the timolol group compared with the placebo group (p less than .01). Also, the mean heart rate during the first 10 days after the acute infarction was reduced by 13% in the timolol group (p less than .001). The reduction in heart rate and left ventricular apical wall motion caused by timolol in patients with acute anterior myocardial infarction may increase the occurrence of left ventricular thrombi.

Circulating catecholamine and potassium concentrations early in acute myocardial infarction: effect of intervention with timolol.

In a prospective study, 20 patients with a first acute myocardial infarction and no current treatment with diuretics or cardioactive drugs were randomized to treatment with intravenous timolol (10 patients) or placebo (10 patients). Plasma adrenaline, noradrenaline, and serum potassium were estimated at baseline (mean +/- SD 3.6 +/- 0.8 hours after the onset of the infarction) and 4 hours after the start of treatment. The patient selection criteria embraced a low-risk study population. Before treatment, the serum potassium concentrations correlated inversely with plasma adrenaline but not with plasma noradrenaline concentrations. A rise of serum potassium (mean +/- SD mmol/L) from 4.1 +/- 0.3 to 4.4 +/- 0.4 (p less than 0.05) in the placebo group and from 4.0 +/- 0.4 to 4.5 +/- 0.5 (p less than 0.05) in the timolol group was in multivariate analysis associated with infarct size, estimated as cumulative creatine kinase release, in the placebo group, and with the mean individual plasma adrenaline concentrations in the timolol group. By reversing the effect of adrenaline from a decrease to an increase in the serum potassium concentrations, timolol changes the relationships between circulating adrenaline, potassium, and infarct size.