bluuebunny/crossref_metadata_2025 huggingface dataset:
Assessment and follow-up of patients with aortic regurgitation by an updated Doppler echocardiographic measurement of the regurgitant fraction in the aortic arch.
Authors: Touche T , Prasquier R , Nitenberg A , de Zuttere D , Gourgon R
Published: June 2011

The purpose of this study was to determine the value and limitations of an updated Doppler echocardiographic measurement of the aortic regurgitant fraction derived from the comparison of forward and reverse flows in the aortic arch. The method was based on the improvements in sampling and displaying Doppler frequencies and blood velocities provided by pulsed-emission, two-dimensional location, and spectral analysis and on an account for variations of aortic diameter through an M mode record of the aortic arch. Relevant statistical comparisons were performed between simultaneous noninvasive and invasive determinations of the regurgitant fraction in a group of 30 patients with aortic regurgitation (group I) and between simultaneous noninvasive and invasive measurements of variations of the regurgitant fraction induced by atrial pacing or vasodilator administration in 12 patients of this group. The two basal determinations were closely correlated (r = .90). The invasive regurgitant fraction ranged from 0% to 80%. The standard error of the Doppler estimate was 8.8% in group I as a whole and was only 6% in a subgroup of 20 patients with a high systolic aortic flow pattern, defined as both peak velocity above 0.8 m/sec and duration of systolic flow above 0.24 sec. This pattern was present in almost all (19/22) patients in whom the aortic regurgitation was more than moderate by invasive criterion (regurgitant fraction above 40%). The standard error of the Doppler estimate of variations of the regurgitant fraction was only 6.6%. Among 100 additional patients with aortic regurgitation (group II), only 12 had no pandiastolic reverse flow in the arch, and their regurgitation was always mild at aortographic examination.(ABSTRACT TRUNCATED AT 250 WORDS)
Importance of internal controls, statistical methods, and side effects in short-term trials of vasodilators: a study of hydralazine kinetics in patients with aortic regurgitation.
Authors: McKay C R , Nana M , Kawanishi D T , Elkayam U , Chandraratna P A , Weiss J N , Rahimtoola S H
Published: June 2011

We determined that the spontaneous changes in cardiac output (CO) over 12 hr in 21 patients with chronic severe aortic regurgitation averaged +/- 8.9% (p = .03). We then measured changes in CO over time after administering incremental doses of oral hydralazine (50, 100, 150, and 200 mg) every 12 hr and analyzed these changes by several methods. Changes over time of only + 14% were highly significant (p less than .001) when analyzed by t test, but were not significant by repeated-measures analysis of variance (ANOVA). When changes in CO were compared with internal control values (spontaneous changes over 12 hr), only changes of 20% or more were significant (p less than .05). Transient "peak effects" markedly overestimated the maximum effects after all doses. We then compared the incremental doses of hydralazine, given either every 8 or every 12 hr, with respect to (1) the hemodynamic changes induced, and (2) the relative incidence of acute side effects. Maximal increases in CO were similar when hydralazine was given every 8 hr (16 patients) and every 12 hr (21 patients), and ranged from + 14% after 50 mg to + 61% after 200 mg. After the 150 and 200 mg doses, marked sustained increases in CO were present at 8 hr and mild increases in CO were still present at 12 hr. Hydralazine every 8 hr was associated with side effects in 25% to 86% of patients, but when the drug was given every 12 hr it was associated with side effects in only 5% to 19% of patients (p less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)
Exercise thallium-201 scintigraphy in dogs: effects of long-term coronary occlusion and collateral development on early and late scintigraphic images.
Authors: Cohen M V , Steingart R M
Published: June 2011

To examine the effects of coronary collateral development on thallium-201 (201Tl) distribution the left circumflex coronary artery was ligated in eight dogs. Three days later these animals ran on a treadmill, and 201-thallous chloride was injected into the right atrium at peak exercise. Scintigraphic scanning was begun within 10 min and continued for 3 hr. Scanning was repeated weekly for 6 weeks. In the last week radioactive microspheres were injected into the left atrium at peak exercise to measure regional myocardial blood flow. The scintigraphically determined disparity between perfusion of the ischemic and normal myocardium was most marked at 3 days after ligation. This difference gradually lessened over the first 4 weeks until there was no difference in 201Tl distribution to normally perfused myocardium and tissue distal to the ligation. Concomitant with the improvement in the scintigrams, exercise hemodynamics also improved over this 4 week period with significant increases in cardiac output and decreases in left atrial pressure. Serial coronary angiographic studies in two animals demonstrated the appearance of collaterals in the initial weeks after coronary occlusion, and by 4 weeks the left circumflex artery distal to the obstruction was completely opacified by collateral flow. The ratio of directly measured exercise blood flow to the left circumflex and normally perfused tissues was 0.89 +/- 0.08 at 6 weeks after ligation. Scintigraphic 201Tl redistribution after 3 hr also changed over the weeks after ligation. Three days after ligation washout from the ischemic area was significantly slower than that from the normal myocardium. By 6 weeks loss of 201Tl from the two regions occurred at nearly equal rates. Thus myocardial perfusion and function during exercise after coronary occlusion are dynamic events that change with time. It is likely that coronary collateral development is responsible for these phenomena. Therefore coronary collaterals do have salutary effects in the dog.
Effects of synthetic atrial natriuretic peptide on renal function and renin release in acute experimental heart failure.
Authors: Scriven T A , Burnett J C
Published: June 2011

Studies were performed in anesthetized control dogs (n = 6) and in dogs (n = 6) with acute low-output heart failure produced by inflation of a balloon in the thoracic inferior vena cava. Studies were designed to determine the effects of synthetic atrial natriuretic peptide on renal function and renin release in this acute high-renin, sodium-retaining preparation. Intrarenal infusion of synthetic atrial natriuretic peptide (0.3 micrograms X kg-1 X min-1) resulted in decreases in arterial pressure and renal blood flow in both groups. Glomerular filtration rate increased in both low-output (delta + 10.7 +/- 3.1 ml/min) and control (delta + 8.7 +/- 2.9 ml/min) groups. Fractional lithium excretion, a marker of proximal tubule reabsorption, also increased in both low-output (delta + 12.0 +/- 4.6%) and control (delta + 14.3 +/- 5.0%) groups. Renin secretory rate decreased in the low-output group from 852.8 +/- 183.0 to 149.5 +/- 73.7 ng/min and in the control group from 308.5 +/- 84.5 to 44.5 +/- 27.5 ng/ml. Intrarenal infusion of atrial natriuretic peptide resulted in an attenuated increase in both urinary sodium excretion (delta + 42.3 +/- 10.7 vs delta + 201.2 +/- 37.9 mueq/min) and fractional excretion of sodium (delta + 0.48 +/- 0.13% vs delta + 2.85 +/- 0.45%) in the low-output as compared with the control group. Our studies demonstrate that administration of synthetic atrial natriuretic peptide results in an increase in glomerular filtration rate and a decrease in proximal tubule reabsorption, as estimated by lithium excretion, in both control dogs and those with acute low-output heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)
In-hospital morbidity and mortality in patients undergoing elective coronary angioplasty.
Authors: Bredlau C E , Roubin G S , Leimgruber P P , Douglas J S , King S B , Gruentzig A R
Published: June 2011

We prospectively recorded all in-hospital complications of the first 3500 consecutive patients to undergo elective coronary angioplasty (PTCA) at Emory University Hospitals from July 14, 1980, to August 28, 1984, by three operators. PTCA was attempted in a total of 3933 lesions, with a primary success rate of 91%. Multiple-lesion PTCA was performed in 401 patients, and PTCA of saphenous vein grafts was attempted in 172. No complications were recorded in 3116 (89%) cases, isolated minor complications occurred in 241 (6.9%), and major complications (emergency surgery, myocardial infarction, death) were observed in 145 (4.1%). Emergency coronary artery bypass graft surgery (CABG) was performed in 96 patients (2.7%), with a myocardial infarction rate of 49% (47/96), a Q wave infarction rate of 23% (22/96), and an emergency surgery mortality rate of 2% (2/96). Hospital discharge occurred within 2 weeks of attempted PTCA in 91% (87/96) of patients undergoing emergency CABG. The overall myocardial infarction rate was 2.6% (94/3500). There were two nonsurgical deaths, giving a total mortality rate of 0.1% (4/3500). Univariate and multivariate analysis of 3099 patients undergoing single-lesion PTCA identified five preprocedure predictors of a major complication: multivessel coronary disease, lesion eccentricity, presence of calcium in the lesion, female gender, and lesion length. Unstable angina, duration of angina, lesion severity, previous CABG, and vein graft dilatation were not associated with an increased incidence of major complications. The strongest predictor of a major complication was the procedural appearance of an intimal dissection. Intimal dissection was evident in 894/3099 (29%) patients.(ABSTRACT TRUNCATED AT 250 WORDS)
Complex ventricular arrhythmias in patients with Q wave versus non-Q wave myocardial infarction.
Authors: Maisel A S , Scott N , Gilpin E , Ahnve S , Le Winter M , Henning H , Collins D , Ross J
Published: June 2011

We examined whether or not subsets of patients with complex ventricular arrhythmias after myocardial infarction are at high risk with respect to 1 year mortality after hospital discharge. Based on previous studies showing increased risk for those with non-Q wave infarcts, we hypothesized that complex PVCs (premature ventricular complexes) in this group might be associated with a poorer prognosis than complex PVCs in patients with Q wave infarcts. Seven hundred seventy-seven patients entering our study with acute infarction were followed prospectively for 1 year after undergoing a predischarge 24 hr ambulatory electrocardiographic examination. Patients were classified by electrocardiographic criteria into the following groups: Non-Q wave (n = 191), Q wave anterior (n = 261), and Q wave inferior infarction (n = 325). The following arrhythmias were classified as complex: multiform PVCs, couplets, and ventricular tachycardia. Sixty-two percent of patients with non-Q wave infarcts who did not survive 1 year had complex PVCs, compared with 32% of survivors (p less than .01). No differences were seen in the Q wave subgroup. The survival for patients with Q wave and non-Q wave infarction without complex PVCs were nearly identical at 1 year (93% and 90%), whereas in patients with complex PVCs survival for those with Q wave and non-Q wave infarction was 92% and 76%, respectively (p less than .001). Of those with non-Q wave infarction, only 4% of nonsurvivors were free of any PVCs, as compared with 28% of nonsurvivors in the Q wave group (p less than .02).(ABSTRACT TRUNCATED AT 250 WORDS)
Isometric exercise in patients with chronic advanced heart failure: hemodynamic and neurohumoral evaluation.
Authors: Elkayam U , Roth A , Weber L , Hsueh W , Nanna M , Freidenberger L , Chandraratna P A , Rahimtoola S H
Published: June 2011

We evaluated the hemodynamic effects of isometric exercise in 53 patients with congestive heart failure (CHF) and compared them with those found in 10 normal subjects. In both groups, isometric exercise increased heart rate and blood pressure. Systemic resistance increased in patients with CHF (1862 +/- 520 vs 2126 +/- 642 dyne-sec-cm-5; p less than .001) but not in normal subjects (1359 +/- 268 vs 1380 +/- 252 dyne-sec-cm-5). Cardiac index and stroke volume index increased mildly but not significantly in the normal subjects (2.8 +/- 0.5 vs 3.1 +/- 0.7 liters/min/m2 and 46 +/- 8 vs 47 +/- 7 ml/m2) and showed a significant fall in the patients with CHF (2.1 +/- 0.6 to 1.9 +/- 0.6 liters/min/m2, p less than .01 and 23 +/- 7 vs 20 +/- 7 ml/m2, p less than .01). Mean pulmonary arterial wedge pressure increased in patients with CHF from 26 +/- 7 to 30 +/- 8 mm Hg (p less than .001). Although no significant change was found in mean value for stroke work index (21 +/- 9 vs 20 +/- 9 g-m/m2), the individual changes were variable, with marked decrease (greater than 15%) in 17 of the patients. This hemodynamic deterioration could not be predicted from resting hemodynamics, left ventricular ejection fraction, or functional classification. Isometric exercise resulted in no significant change in circulatory catecholamine levels or plasma renin concentration in our 10 normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
Pharmacology of platelet inhibition in humans: implications of the salicylate-aspirin interaction.
Authors: de Gaetano G , Cerletti C , Dejana E , Latini R
Published: June 2011

The current dispute over the effects of "low" vs "high" doses of aspirin should take into consideration the pharmacokinetics of this drug. In fact, different pharmaceutical formulations of aspirin may deliver little or no aspirin to the systemic blood. This was the case, for instance, in healthy volunteers taking 320 mg of compressed aspirin or 800 mg of enteric-coated aspirin. In all instances thromboxane B2 generation in serum was fully inhibited. Platelet cyclooxygenase might therefore be effectively acetylated by exposure to aspirin in the portal circulation, whereas vascular cyclooxygenase could be spared. Thus aspirin formulations ensuring complete first-pass deacetylation should be sought rather than "low" or "high" doses of unspecified aspirin formulations. Regardless of the type and dose of aspirin administered, salicylate is formed and accumulates in the circulation. It may antagonize the effects of aspirin on cyclooxygenase, at least in acute conditions. As an example, after administration of 1 g of salicylate to healthy volunteers, when plasma levels of the drug were about 75 micrograms/ml, the effect of 40 mg iv aspirin (given 40 min later) on platelet cyclooxygenase and aggregation was significantly diminished. In contrast, in patients undergoing saphenectomy, the same dose of salicylate (1 g) gave plasma drug levels of about 25 micrograms/ml; salicylate was unable to prevent the inhibitory effect on platelets of 40 mg iv aspirin (given 1 hr later) but did act on vascular prostacyclin. Thus the combination of salicylate with aspirin at an appropriate dose and blood level ratio may result in almost complete dissociation of the drug's effect on platelets and vessels in man.(ABSTRACT TRUNCATED AT 250 WORDS)
The pressure-flow response of the pulmonary circulation in patients with heart failure and pulmonary vascular disease.
Authors: Janicki J S , Weber K T , Likoff M J , Fishman A P
Published: June 2011

Although it is well known that the pulmonary circulation is altered in patients with pulmonary arterial or venous hypertension, the resultant hemodynamic behavior has not been systematically studied. We undertook to do so in a group of patients with pulmonary hypertension of diverse etiology. We measured pulmonary arterial (PAP) and occlusive wedge pressures and cardiac output at rest (i.e., standing) and during progressive upright treadmill exercise in 51 patients. Forty-two had chronic, stable, cardiac failure secondary to ischemic, myopathic or valvular heart disease and were grouped according to whether their mean PAP was less than (normotensive) or greater than (hypertensive) 19 mm Hg, and nine had pulmonary vascular disease of diverse etiology and were considered separately. In the majority of patients, we found that irrespective of whether the hypertension was arterial or venous in origin or etiology: the mean PAP-flow relationship was linear; pulmonary capillary wedge pressure was greater than or equal to the average closure pressure of the pulmonary vascular bed and could therefore be used as the downstream pressure in calculating pulmonary vascular resistance; and pulmonary vascular resistance declined with exercise. Notable exceptions to the third observation were patients with valvular heart disease or a resting pulmonary vascular resistance greater than 800 dyne-sec-cm-5.
Myocardial thallium-201 kinetics during coronary occlusion and reperfusion: influence of method of reflow and timing of thallium-201 administration.
Authors: Granato J E , Watson D D , Flanagan T L , Gascho J A , Beller G A
Published: June 2011

Thallium-201 (201Tl) uptake and redistribution kinetics were examined in an open-chest canine preparation of occlusion and reperfusion. Seven dogs (group I) underwent 3 hr of sustained occlusion and received 1.5 mCi of 201Tl after 40 min of occlusion of the left anterior descending coronary artery (LAD). Group II (n = 18) underwent 60 min of LAD occlusion followed by sudden and total release of the ligature. Group IIa (n = 8) received intravenous 201Tl during occlusion of the LAD, whereas group IIb (n = 10) received intravenous 201Tl at the time of peak reflow. Group III dogs (n = 26) also underwent 60 min of LAD occlusion that was followed by gradual reflow through a residual critical stenosis. Animals in this group also received 201Tl either before (IIIa; n = 16) or after reflow was established (IIIb; n = 10). In group I, the relative 201Tl gradient (nonischemic minus ischemic activity) decreased from 88 +/- 8% (mean +/- SEM) to 59 +/- 6% during 3 hr of coronary occlusion (p = .034). After rapid and total reperfusion (group IIa), this gradient decreased from 71 +/- 6% during occlusion to 26 +/- 5% after reflow (p less than .001). After slow reperfusion through a residual stenosis (group IIIa), the gradient decreased from 81 +/- 5% to 31 +/- 5% (p less than .001) (p = .56 compared with group IIa). In rapidly reperfused dogs receiving intravenous thallium during peak reflow (IIb), initial 201Tl activity in the ischemic zone was 155 +/- 20% of initial normal activity and fell to 93 +/- 13% of normal after 2 hr of reperfusion. Similarly, in dogs reperfused slowly through a critical stenosis (IIIb), which received 201Tl during reflow, 201Tl activity soon after reflow was 94 +/- 4% of initial normal and decreased to 80 +/- 6% at 2 hr of reperfusion (p = .10). Histochemical evidence of necrosis was present in the biopsy region in 80% of the 20 dogs subjected to triphenyl tetrazolium chloride (TTC) staining. Microsphere-determined transmural blood flow was similar in all groups during LAD occlusion and final flows after 2 hr were comparable in all subgroups undergoing reflow. Ischemic zone flow (% normal) was significantly higher at the time of 201Tl administration in groups IIb (192 +/- 25%) and IIIb (110 +/- 5%), which received 201Tl during reflow, than in groups IIa (31 +/- 9%) and IIIa (22 +/- 5%), which received 201Tl during occlusion.(ABSTRACT TRUNCATED AT 400 WORDS)
The effect of contractility and preload on matching between the canine left ventricle and afterload.
Authors: Myhre E S , Johansen A , Bjørnstad J , Piene H
Published: June 2011

We define matching between ventricle and afterload to imply that the ventricle is adapted to its afterload to yield maximum external work output. For the ventricle, this optimal adaption will depend on end-diastolic dimension, heart rate, and contractility. Because contractility is impaired during ventricular failure, we propose that the adaption between ventricle and load is not as good during failure as during normal conditions. According to our definition, this implies that during failure external work output is less than maximum. Ventricle-load matching is then not present, i.e., a mismatch exists between ventricle and load. This hypothesis was tested in a canine preparation in which arterial load of the left ventricle was varied from one beat to the next. Left ventricular depression was induced by injections of 50 micron microspheres into the left coronary bed. We observed left ventricular stroke volume and external work during afterload variations at three different preload levels before and after microembolization. Before embolization the control observations of work and stroke volume were positioned at the apex of parabolas relating work to stroke volume. After embolization, however, control observations fell down along the left limb of the parabolas. These observations were independent of preload. Thus this study, carried out in a preparation with the heart in situ, supports the idea that the normal left ventricle is matched to its load and demonstrates ventricle-load mismatch when the left ventricle is failing.
Absence of left ventricular dysfunction during acute chagasic myocarditis in the rhesus monkey.
Authors: Lima J A , Szarfman A , Lima S D , Adams R J , Russell R J , Cheever A , Trischmann T , Weiss J L
Published: June 2011

Recent studies suggest that intracellular Trypanosoma cruzi invasion with release of intracellular myocardial antigens during T. cruzi infection is crucial to the pathogenesis of chronic chagasic myocarditis. However, in areas endemic for Chagas' disease, the incidence of clinical acute chagasic myocarditis has been reported to be low among infected individuals, while the incidence of chronic chagasic myocarditis is relatively high. Thus, either acute chagasic myocarditis rarely complicates T. cruzi infection and is not important to the pathogenesis of chronic chagasic myocarditis, or acute chagasic myocarditis rarely impairs left ventricular function and therefore causes no symptoms. To investigate this question we innoculated T. cruzi from a human patient with Chagas' disease into the subconjuntivae of six rhesus monkeys (7.5 X 10(3) parasites each). Parasitemia was monitored and weekly two-dimensional echocardiograms (for determination of end-diastolic and fractional change in area, EDA and FCA) were obtained to quantify global left ventricular function for 10 weeks. Regional left ventricular function was assessed by visual analysis of two-dimensional echocardiograms. Extent of acute myocarditis was established at autopsy. All monkeys had the Romaña sign and detectable parasitemia in the second week. Parasitemia rose in all by the ninth week (mean = 1.8 X 10(5) parasites/ml); four monkeys lost weight (mean = -12%), three died, and three were killed. Two-dimensional echocardiographic EDA and FCA remained unchanged from control to the last study within 12 hr of death (EDA = 2.6 +/- 0.9 to 2.7 +/- 1.0 cm2, FCA = 80 +/- 6.8 to 74 +/- 7.6%, NS). Furthermore, regional left ventricular function remained unchanged throughout the period of study.(ABSTRACT TRUNCATED AT 250 WORDS)
Pulsed Doppler findings in patients with coarctation of the aorta.
Authors: Shaddy R E , Snider A R , Silverman N H , Lutin W
Published: June 2011

We used combined two-dimensional and pulsed Doppler echocardiography to examine 37 infants and children with coarctation of the aorta and 19 normal subjects. The ages ranged from 1 day to 16 years. We compared the differences between the Doppler flow signal from the ascending aorta and the descending aorta below the coarctation in each patient, as well as the differences between the corresponding flow signals in the aorta of patients with coarctation and normal subjects. Six variables were measured from each Doppler signal: acceleration slope (peak rate of acceleration), acceleration time (time from onset of flow to the peak systolic frequency), antegrade flow time, peak systolic frequency, peak velocity of flow, and deceleration slope (peak rate of deceleration). In patients with coarctation, each of these variables was significantly different in the descending aorta compared with the ascending aorta. There was a decrease in the acceleration slope (14 +/- 13 vs 87 +/- 67 kHz/sec) (mean +/- SD), peak systolic frequency (1.8 +/- 1.0 vs 5.2 +/- 1.9 kHz), peak velocity of flow (0.70 +/- 0.40 vs 1.4 +/- 0.44 m/sec), and deceleration slope (11 +/- 11 vs 27 +/- 12 kHz/sec). There was also a prolongation of the acceleration time (140 +/- 50 vs 88 +/- 22 msec) and antegrade flow time (330 +/- 120 vs 270 +/- 50 msec). In addition, these variables in the descending aorta of patients with coarctation were significantly different from those in the descending aorta of normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
Pathophysiology of coronary occlusion in acute infarction.
Authors: Maseri A , Chierchia S , Davies G
Published: June 2011

Coronary angiography has proved beyond doubt that complete coronary occlusion is the rule in the very early hours of infarction. The 60% to 80% rate of coronary recanalization after thrombolytic therapy has proved that thrombosis is a major component of the occlusion at the time when the procedure is performed a few hours after the onset of symptoms. However, the trigger for coronary thrombosis and the causes of failure of thrombolytic therapy are still a matter of speculation. The relatively rare occurrence of acute coronary occlusion in the life of an individual with even severe coronary disease can be explained on the basis of the necessity of either extremely powerful isolated stimuli, which only occurs rarely, or the casual simultaneous presence in one coronary arterial segment of multiple unfavorable events, such as plaque fissuring, enhanced reactivity of coronary smooth muscle to constrictor stimuli and displacement of the thrombotic-thrombolytic equilibrium toward thrombosis. Coronary artery constriction possibly caused by vasoconstrictor substances released by thrombus, represents the potential element of a vicious cycle causing persistent coronary occlusion and reocclusion when reflow occurs with thrombolysis.
Echocardiographic assessment of the evolution of amyloid heart disease: a study with familial amyloid polyneuropathy.
Authors: Hongo M , Ikeda S
Published: June 2011

To determine the evolution of amyloid heart disease, 28 patients with familial amyloid polyneuropathy (FAP) were studied by echocardiography. The incidence and degree of the abnormalities were correlated with the neurologic disabilities, duration of the illness, and age in cross-sectional studies. Serial studies were performed in 12 patients, who were followed for a mean of 27.7 months. At the initial examinations, left ventricular diastolic function was reduced in six patients, while systolic function was preserved in eight. On follow-up there occurred significant increases in ventricular septal wall thickness (from 10.7 +/- 3.1 to 13.1 +/- 3.2 mm; p less than .01) and posterior wall thickness (from 11.8 +/- 2.5 to 13.5 +/- 2.3 mm; p less than .01), and reductions in the E-F slope of the mitral valve (from 64.4 +/- 18.8 to 43.9 +/- 11.0 mm/sec; p less than .01), percent fractional shortening (from 36.5 +/- 9.4% to 28.8 +/- 8.2%; p less than .02), and left ventricular internal diastolic dimension (from 46.2 +/- 6.1 to 42.4 +/- 6.2 mm; p less than .001). At the final examinations, marked ventricular hypertrophy was found in three patients, reduced left ventricular diastolic function in all, impaired systolic function in nine, and decreased left ventricular internal dimension in three. In addition, highly refractile myocardial echoes had appeared in two patients, pericardial effusion in three, and valve thickening in two. We conclude that amyloid heart disease in patients with FAP develops slowly but progressively.
The effects of cyclosporine on acute murine Coxsackie B3 myocarditis.
Authors: O'Connell J B , Reap E A , Robinson J A
Published: June 2011

The effects of the immunosuppressant drug cyclosporine were studied in the murine model of Coxsackie B3 myocarditis. Ten BALB/c mice, given daily cyclosporine (15 mg/kg) intraperitoneally but not infected, were normal in all respects after 2 weeks. All 32 BALB/c mice infected, but given no cyclosporine, survived and had moderate myocardial mononuclear infiltrates and minimal necrosis at 7 and 14 days. In contrast, 24 mice concurrently infected and given cyclosporine had a high mortality rate (75%) and a significantly attenuated mononuclear infiltrate in the presence of enhanced necrosis when compared with control infected mice. Sixteen mice started on the drug 1 week after infection had a lower mortality rate (55%), but very similar histologic abnormalities. In contrast to negligible or no virus in the hearts of infected mice that were not given cyclosporine, drug treated, infected groups had easily detectable virus in their hearts 14 days after infection. An identical study in Swiss ICR mice yielded similar results. Cyclosporine, when given early during acute murine Coxsackie B3 myocarditis, causes a significant increase in myocardial necrosis and mortality, possibly secondary to enhanced viral survival.
Intramyocardial platelet aggregation in patients with unstable angina suffering sudden ischemic cardiac death.
Authors: Davies M J , Thomas A C , Knapman P A , Hangartner J R
Published: June 2011

A specific search for intramyocardial platelet aggregates was made in 90 patients who died suddenly of ischemic heart disease. Platelet aggregates in small intramyocardial vessels were found in 27 (30%). There was a significant difference (p less than .05) in the incidence of platelet aggregates in patients with chest pain of recent onset (unstable angina) before death (16/36, 44.4%) and that in those without it (11/54, 20.4%). Multifocal microscopic necrosis with involvement of the full thickness of the ventricular wall, including the subpericardial zone, was significantly more common (p = less than .005) in the patients with platelet emboli (55.6% vs 12.7%). With one exception, aggregates were confined to the segment of myocardium immediately downstream of a major epicardial coronary artery containing an atheromatous plaque that had undergone fissuring and on which mural thrombus had developed. The results support the view that platelet aggregates in the myocardium represent an embolic phenomenon and are a potential cause of unstable angina. The association of myocardial necrosis with such emboli could precipitate sudden death from ventricular fibrillation.
Intracoronary papaverine: an ideal coronary vasodilator for studies of the coronary circulation in conscious humans.
Authors: Wilson R F , White C W
Published: June 2011

An ideal coronary vasodilator for studying coronary flow reserve in humans would rapidly produce maximal coronary vasodilation, be short acting to permit repeated measurements, and not alter systemic hemodynamics. The two commonly used vasodilators (dipyridamole and meglumine diatrizoate) do not satisfy these criteria; meglumine diatrizoate does not produce maximal hyperemia and dipyridamole has a long duration of effect (greater than 30 min). In this study we used a subselective coronary Doppler catheter to measure the dose-response kinetics of a shorter acting vasodilator, intracoronary papaverine. In 10 patients with normal coronary vessels, the maximal vasodilator response to papaverine was compared with that to intravenous dipyridamole (0.56 mg/kg infused over 4 min) and intracoronary meglumine diatrizoate. The increase in coronary blood flow velocity after the maximal dose of papaverine (4.8 +/- 0.4 peak/resting velocity ratio, mean +/- SEM) was nearly identical to that seen after infusion of dipyridamole (4.8 +/- 0.6) and was significantly greater than that after meglumine diatrizoate (3.1 +/- 0.2, p less than .01). At maximal hyperemia, mean arterial blood pressure fell 9 +/- 2% (mean +/- SEM) after intracoronary papaverine, 8 +/- 4% after dipyridamole, and 3 +/- 3% after meglumine diatrizoate. The dose-response kinetics of intracoronary papaverine were studied in 13 patients with normal coronary arteries. In the left coronary artery, maximal vasodilation (5.4 +/- 0.6) was achieved with 8 mg in six of eight patients and with 12 mg in all patients. In the right coronary artery, maximal vasodilation (4.8 +/- 0.7) was achieved with 6 mg in four or five patients and with 8 mg in all patients.(ABSTRACT TRUNCATED AT 250 WORDS)
Effect of propranolol after acute myocardial infarction in patients with congestive heart failure.
Authors: Chadda K , Goldstein S , Byington R , Curb J D
Published: June 2011

The incidence of congestive heart failure was studied in the Beta Blocker Heart Attack Trial in which postmyocardial infarction patients between the ages of 30 and 69 years, with no contraindication to propranolol, were randomly assigned to receive placebo (n = 1921) or propranolol 180 or 240 mg daily (n = 1916) 5 to 21 days after admission to the hospital for the event. Survivors of acute myocardial infarction with compensated or mild congestive heart failure, including those on digitalis and diuretics, were included in the study. A history of congestive heart failure before randomization characterized 710 (18.5%) patients: 345 (18.0%) in the propranolol group and 365 (19.0%) in the placebo group. The incidence of definite congestive heart failure after randomization and during the study was 6.7% in both groups. In patients with a history of congestive heart failure before randomization, 51 of 345 (14.8%) in the propranolol group and 46 of 365 (12.6%) in the placebo group developed congestive heart failure during an average 25 month follow-up. In the patients with no history of congestive heart failure, 5% in the propranolol group developed congestive heart failure and 5.3% in the placebo group developed congestive heart failure. Baseline characteristics predictive of the occurrence of congestive heart failure by multivariate analyses included an increased cardiothoracic ratio, diabetes, increased heart rate, low baseline weight, prior myocardial infarction, age, and more than 10 ventricular premature beats per hour.(ABSTRACT TRUNCATED AT 250 WORDS)
Reduction of the size of infarction by allopurinol in the ischemic-reperfused canine heart.
Authors: Werns S W , Shea M J , Mitsos S E , Dysko R C , Fantone J C , Schork M A , Abrams G D , Pitt B , Lucchesi B R
Published: June 2011

This study was performed to assess the effect of allopurinol in a canine preparation of myocardial infarction. Dogs underwent occlusion of the left circumflex coronary artery for 90 min, followed by reperfusion for 6 hr. Three groups were studied: (1) control, (2) dogs receiving 25 mg/kg allopurinol 18 hr before occlusion and 50 mg/kg 5 min before occlusion, and (3) dogs receiving allopurinol as above plus 5 mg/kg superoxide dismutase over 1 hr beginning 15 min before reperfusion. Infarct size expressed as a percentage of the area at risk was 40 +/- 4 in the control group, 22 +/- 5 in the allopurinol group (p less than .05 vs control), and 17 +/- 4 in the allopurinol plus superoxide dismutase group (p less than .05 vs control). The differences in infarct size were not due to differences in myocardial oxygen supply or demand. Neutrophil superoxide anion production was not altered by allopurinol treatment. The results suggest that myocardial xanthine oxidase may generate oxygen radicals that play a role in myocardial injury due to ischemia and reperfusion.
Determinants of blood flow to vital organs during cardiopulmonary resuscitation in dogs.
Authors: Halperin H R , Tsitlik J E , Guerci A D , Mellits E D , Levin H R , Shi A Y , Chandra N , Weisfeldt M L
Published: June 2011

Whether blood flow during cardiopulmonary resuscitation (CPR) results from intrathoracic pressure fluctuations or direct cardiac compression remains controversial. From modeling considerations, blood flow due to intrathoracic pressure fluctuations should be insensitive to compression rate over a wide range, but dependent on the applied force and compression duration. If direct compression of the heart plays a major role, however, flow should be dependent on compression rate and force, but above a threshold, insensitive to compression duration. These differences in hemodynamics produced by changes in rate and duration form a basis for determining whether blood flow during CPR results from intrathoracic pressure fluctuations or from direct cardiac compression. Manual CPR was studied in eight anesthetized, 21 to 32 kg dogs after induction of ventricular fibrillation. There was no surgical manipulation of the chest. Myocardial and cerebral blood flows were determined with radioactive microspheres. At nearly constant peak sternal force (378 to 426 newtons), flow was significantly increased when the duration of compression was increased from 14 +/- 1% to 46 +/- 3% of the cycle at a rate of 60/min. Flow was unchanged, however, after an increase in rate from 60 to 150/min at constant compression duration. The hemodynamics of manual CPR were next compared with those produced by vest inflation with simultaneous ventilation (vest CPR) in eight other dogs. Vest CPR changed intrathoracic pressure without direct cardiac compression, since sternal displacement was less than 0.8 cm. At a rate of 150/min, with similar duration and right atrial peak pressure, manual and vest CPR produced similar flow and perfusion pressures. Finally, the hemodynamics of manual CPR were compared with the hemodynamics of direct cardiac compression after thoracotomy. Cardiac deformation was measured and held nearly constant during changes in rate and duration. As opposed to changes accompanying manual CPR, there was no change in perfusion pressures when duration was increased from 15% to 45% of the cycle at a constant rate of 60/min. There was, however, a significant increase in perfusion pressures when rate was increased from 60 to 150/min at a constant duration of 45%. Thus, vital organ perfusion pressures and flow during manual external chest compression are dependent on the duration of compression, but not on rates of 60 or 150/min. These data are similar to those observed for vest CPR, where intrathoracic pressure is manipulated without sternal displacement, but opposite of those observed for direct cardiac compression.(ABSTRACT TRUNCATED AT 400 WORDS)
Wall thickness, cavity dimensions, and myocardial contractility of the left ventricle in patients with simple transposition of the great arteries. A multicenter study of patients from 10 to 20 years of age.
Authors: Carceller A M , Fouron J C , Smallhorn J F , Cloez J L , van Doesburg N H , Mauran P , Ducharme G , Pernot C , Davignon A
Published: June 2011

Fifty-one patients with uncomplicated transposition of the great arteries (TGA) and normal pulmonary pressure who were 10 to 20 years old and 69 normal subjects matched for age were studied by M mode echocardiography. Left ventricular internal dimensions and posterior wall thickness showed positive correlation with the body surface area in the TGA as well as in the control groups. Values for these parameters in the TGA group were generally smaller than those in the normal population. Septal thickness of patients with TGA (5.9 +/- 1 mm) was also smaller than that in the control group (6.6 +/- 1 mm) (p less than .01). Septal motion was normal in 11 patients with TGA and paradoxical in 19 patients in this group. In the other 21 patients the septum was flat. The following systolic time intervals of the left ventricle were found for patients with TGA: preejection period (PEP) 64 +/- 11 msec, ejection time (ET) 310 +/- 37 msec, and PEP/ET 0.21 +/- 0.04. These values were significantly different from those of the right ventricle for the normal population: PEP 77 +/- 12 (p less than .01), ET 327 +/- 25 (p less than .05), and PEP/ET 0.24 +/- 0.03 (p less than .01). Shortening fraction and mean velocity of circumferential fiber shortening (49 +/- 7% and 1.6 +/- 0.3 circ/sec, respectively) were also significantly higher (p less than .01) in patients with TGA than in the control group (33 +/- 4% and 1.1 +/- 0.2 circ/sec). These data should help achieve reliable quantitative and qualitative interpretations of echocardiograms of patients with TGA.
The relationships between alcoholic beverage use and other traits to blood pressure: a new Kaiser Permanente study.
Authors: Klatsky A L , Friedman G D , Armstrong M A
Published: June 2011

In a new study controlled for many factors, we reconfirmed the relationship of higher blood pressure to alcohol use. This relationship was slightly stronger in men, whites, and persons 55 years of age or older. A slight increase in blood pressure appeared in men who drank one to two drinks daily, and a continuous increase occurred at all higher drinking levels among white men who had constant drinking habits. Among women, an increase occurred only at three or more drinks daily. The data suggest complete regression, beginning within days, of alcohol-associated hypertension upon abstinence. Blood pressure showed minor differences with beverage preference: those who preferred liquor had higher adjusted mean blood pressure than those preferring wine or beer. The results of this study contribute to the likelihood that the alcohol-blood pressure association is causal. Smoking, coffee use, and tea use showed no association with higher blood pressure. Systolic pressure showed a positive relationship to total serum calcium and an inverse relationship to serum potassium, but diastolic pressure showed little relationship to these blood constituents; the explanations include a possible direct effect on regulation of blood pressure.
The coronary circulation in human septic shock.
Authors: Cunnion R E , Schaer G L , Parker M M , Natanson C , Parrillo J E
Published: June 2011

Reversible myocardial depression, manifested by ventricular dilatation and decreased ejection fraction, is common in human septic shock. A proposed mechanism, based on animal studies, is myocardial ischemia resulting from inadequate coronary blood flow. Coronary flow observations have not been reported for human septic shock. To determine whether myocardial depression in human septic shock is associated with reduced coronary flow, thermodilution coronary sinus catheters were placed in seven patients with septic shock for measurements of coronary flow and myocardial metabolism. Four of the seven patients developed myocardial depression. These patients had coronary flow similar to or higher than that of control subjects and similar to that of the other three patients, who did not develop myocardial depression. None of the patients had net myocardial lactate production. In general, compared with values in control subjects, the oxygen content difference (arterial minus coronary sinus) was narrowed, and the fractional extraction of arterial oxygen was diminished. This pattern of disordered coronary autoregulation is analogous to the pattern of arteriovenous shunting in other organs in patients with septic shock. The preservation of coronary flow, the net myocardial lactate extraction, and the increased availability of oxygen to the myocardium argue against global ischemia as the cause of myocardial depression in human septic shock.
Incomplete lysis of thrombus in the moderate underlying atherosclerotic lesion during intracoronary infusion of streptokinase for acute myocardial infarction: quantitative angiographic observations.
Authors: Brown B G , Gallery C A , Badger R S , Kennedy J W , Mathey D , Bolson E L , Dodge H T
Published: June 2011

Thrombolytic recanalization of the obstructed coronary lumen was studied in 32 patients receiving intracoronary streptokinase for 60 to 90 min during acute myocardial infarction. The process was viewed at high arteriographic magnification and was quantified with computer-assisted measurements from repeated single-plane views. The variability of the method for this application was 0.15 to 0.18 mm on minimum diameter estimates. Structural details were seen that are not commonly appreciated at conventional magnification. The recanalized lumen appears to form along an interface between the thrombus and the vessel wall, progressively enlarging its minimum arteriographic diameter to 0.65 +/- 0.24 mm (+/- 1 SD) at the end of the short-term infusion of streptokinase reflecting a final percent stenosis of 77 +/- 10%. In nine infarct lesions found patent 5 +/- 3 weeks later, the recanalized lumen further improved an average of 0.34 mm in minimum diameter (p less than .005) and 13% stenosis (p less than .01). A thin film of contrast medium surrounding the obstructing thrombus faintly defined the boundaries of the original atherosclerotic lumen in all but two cases. The "original stenosis" measured 1.25 +/- 0.32 mm in minimum diameter and 56 +/- 14% stenosis when first visualized; it was unchanged throughout the course of infusion of streptokinase. In five patients catheterized 10 +/- 12 weeks before their infarction, the original stenosis averaged 1.15 +/- 0.22 mm in the preinfarct angiogram, as compared with 1.17 +/- 0.23 mm in its faintly defined form during thrombolytic therapy (p = NS). In 10 cases, this original lesion was less than a 50% stenosis, and in 21 cases less than 60%.(ABSTRACT TRUNCATED AT 250 WORDS)
A clinicopathologic study of patients with hemorrhagic myocardial infarction treated with selective coronary thrombolysis with urokinase.
Authors: Fujiwara H , Onodera T , Tanaka M , Fujiwara T , Wu D J , Kawai C , Hamashima Y
Published: June 2011

Hemorrhagic acute myocardial infarction (AMI) was studied after selective intracoronary thrombolysis (SICT) in 30 patients undergoing autopsy. Urokinase, 240,000 to 1,200,000 U, was selectively injected into the infarct-related coronary artery at 2 to 9 hr (4 +/- 2 hr) after the onset of AMI. The infarct-related coronary artery showed complete occlusion in 21, 99% stenosis in eight, and 90% stenosis in one patient before SICT. After SICT, complete occlusion was seen in only five, 99% stenosis in 22, and 90% stenosis in three patients. Twenty-eight patients had transmural infarction and the other two had subendocardial infarction. Macroscopically and microscopically, the degree of hemorrhage was classified as no, slight, moderate, or marked bleeding and the hemorrhagic infarction was defined as moderate or marked diffuse bleeding in the infarct area. According to the interval from SICT to death, patients were also classified into stage I (early acute stage, 1 to 4 hr after SICT and 4 to 13 hr after the onset of AMI; n = 7), stage II (late acute stage, 9 hr to 11 days after SICT and 15 hr to 11 days after the onset of AMI; n = 18), or stage III (old infarction stage, over 17 days after AMI and SICT; n = 5). There were no significant differences with respect to the frequency of recanalization, the time from the onset of AMI to SICT, the dose of urokinase, or other clinical parameters among patients at the three stages. Only the hearts of patients in stage II showed hemorrhagic infarction, and it was found in 15 of 18 of these hearts.(ABSTRACT TRUNCATED AT 250 WORDS)