bluuebunny/crossref_metadata_2025 huggingface dataset:
Diagnosis of coronary artery disease by controlled coronary vasodilation with adenosine and thallium-201 scintigraphy in patients unable to exercise.
Authors: Verani M S , Mahmarian J J , Hixson J B , Boyce T M , Staudacher R A
Published: June 2011

Pharmacological coronary vasodilation induced by dipyridamole is often used in association with thallium-201 myocardial scintigraphy to evaluate the presence and prognostic significance of coronary artery disease. Because dipyridamole acts by blocking the cellular uptake of adenosine, we investigated the usefulness of direct intravenous administration of adenosine, a physiological substance with an exceedingly short (less than 2 seconds) plasma half-life, to induce maximal controlled coronary vasodilation in conjunction with 201Tl scintigraphy. We studied 89 patients (44 men and 45 women; mean age, 64 +/- 10 years [SD]) who were unable to perform an exercise test and were referred for evaluation of suspected coronary artery disease. The intravenous infusion of adenosine began at an initial rate of 50 micrograms/kg/min and was increased by stepwise increments every minute to a maximal rate of 140 micrograms/kg/min. 201Tl was injected intravenously after 1 minute at the highest infusion rate, followed by immediate and delayed (4 hour) tomographic imaging. At the highest infusion rate, adenosine induced a significant (p less than 0.001) decrease in systolic (8.7 +/- 19.3 mm Hg) and diastolic (6.7 +/- 9.4 mm Hg) blood pressures as well as a significant (p = 0.0001) increase in heart rate (14.5 +/- 11.0 beats/min). Side effects occurred in 83% of the patients but resolved spontaneously within 1 or 2 minutes after discontinuing the adenosine infusion. Chest, throat, or jaw pain were the most frequent symptoms and occurred in 57% of the patients. Headache (35%) and flush (29%) were also common. Ischemic electrocardiographic changes occurred in 12% of the patients, and transient first-degree atrioventricular block occurred in 10%.(ABSTRACT TRUNCATED AT 250 WORDS)
Restrictive diastolic abnormalities identified by Doppler echocardiography in patients with thalassemia major.
Authors: Spirito P , Lupi G , Melevendi C , Vecchio C
Published: June 2011

The consequences of transfusional iron overload on left ventricular diastolic filling have never been investigated systematically in patients with thalassemia major. In the present study, the pattern of left ventricular filling was assessed by Doppler echocardiography in 32 patients with thalassemia major (age, 17 +/- 5 years) who had not experienced symptoms of heart failure and had normal left ventricular systolic function. Data were compared with those obtained in 32 age-matched and sex-matched normal subjects. An abnormal Doppler pattern of left ventricular filling with increased flow velocity at mitral valve opening followed by an abrupt and premature decrease of flow velocity in early diastole was identified in the patients with thalassemia. Peak flow velocity in early diastole was increased in patients compared with controls (90 +/- 10 vs. 81 +/- 15 cm/sec; p less than 0.01), and rate of deceleration of flow velocity after the early diastolic peak and the ratio between the early and late (atrial) peaks of flow velocity were also increased (1,050 +/- 325 vs. 762 +/- 193 cm/sec2 and 2.7 +/- 0.7 vs. 2.2 +/- 0.5, respectively; p less than 0.001), whereas flow velocity deceleration time was reduced (97 +/- 22 vs. 119 +/- 19 msec; p less than 0.001). This Doppler pattern of diastolic filling is usually described as "restrictive" and reflects a decrease in left ventricular chamber compliance. A restrictive pattern of left ventricular filling was also identified in the subgroup of 16 study patients who had undergone optimal iron chelation therapy with deferoxamine.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiac abnormalities in systemic lupus erythematosus. Association with raised anticardiolipin antibodies.
Authors: Nihoyannopoulos P , Gomez P M , Joshi J , Loizou S , Walport M J , Oakley C M
Published: June 2011

Two-dimensional echocardiographic studies were prospectively performed in 93 patients with systemic lupus erythematosus (SLE) to discover the incidence and spectrum of cardiac abnormalities and to relate these findings to the presence of high levels of anticardiolipin antibodies. Assessment of the intracardiac anatomy was also performed in an additional 12 patients who had increased anticardiolipin antibody levels but did not have SLE. Fifty patients (54%) with SLE had cardiac abnormalities, and 43 patients (46%) had normal hearts. Three categories of cardiac abnormalities were identified--valvular lesions, ranging from vegetations to valvular thickening, were found in 28%, pericardial effusion or thickening was found in 20%, and regional or global left ventricular dysfunction was found in 5%. High levels of anticardiolipin antibodies were detected in 50 patients (54%) with SLE. Of those, only 11 (22%) had an entirely normal heart, whereas the remaining 39 (78%) had at least one cardiac abnormality (valvular lesions in 20, pericardial effusion in 15, and myocardial dysfunction in five patients). In patients with SLE, the presence of abnormal intracardiac anatomy was strongly associated with increased levels of anticardiolipin antibodies (p less than 0.0001). The overall sensitivity and specificity of high levels of anticardiolipin antibodies in the prediction of cardiac abnormalities was 78% and 74%, respectively, with a positive predictive accuracy of 78% and a negative predictive accuracy of 74%. Eight of the 12 patients (67%) who had increased anticardiolipin antibodies but whose disease did not fulfill the American Rheumatism Association classification criteria for SLE had cardiac abnormalities similar to those in patients with SLE compared with only four (33%) who had normal hearts (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
Intravenous recombinant tissue-type plasminogen activator in patients with unstable angina pectoris. Results of a placebo-controlled, randomized trial.
Authors: Williams D O , Topol E J , Califf R M , Roberts R , Mancini G B , Joelson J M , Ellis S G , Kleiman N S
Published: June 2011

Because thrombus formation may contribute to coronary obstruction in patients with unstable angina pectoris, we performed a pilot investigation to determine whether thrombolytic therapy can relieve coronary narrowing in this acute ischemic syndrome. Sixty-seven patients with rest angina and angiographic evidence of coronary stenosis were randomly assigned to receive either low-dose intravenous recombinant tissue-type plasminogen activator (rt-PA) (0.75 mg/kg over 1 hour), high-dose intravenous rt-PA (0.75 mg/kg over 1 hour; total dose, 100 mg over 6 hours), or intravenous placebo followed by repeat coronary angiography at 24-48 hours to assess change in the severity of coronary narrowing. Each patient also received oral aspirin and intravenous heparin. Mean values of coronary stenosis severity (percent of diameter reduction) declined to a similar extent in each group: placebo, 75 +/- 14% to 72 +/- 14% (p = 0.07); low-dose rt-PA, 75 +/- 16% to 71 +/- 18% (p = 0.03), and high-dose rt-PA, 82 +/- 11% to 77 +/- 17% (p = 0.18), with only the low-dose rt-PA group achieving statistical significance. Resolution of intracoronary filling defects, increase in antegrade flow grade, or both also occurred equally among the three groups. There was considerable variation in individual patient response. Between 29% and 50% of patients within each group demonstrated a decrease in stenosis severity, whereas 50% to 57% noted either improvement in antegrade flow or resolution of intracoronary thrombus. There was no difference in incidence of major bleeding events among the three groups.(ABSTRACT TRUNCATED AT 250 WORDS)
Adjuvant therapy for intracoronary stents. Investigations in atherosclerotic swine.
Authors: Rodgers G P , Minor S T , Robinson K , Cromeens D , Woolbert S C , Stephens L C , Guyton J R , Wright K , Roubin G S , Raizner A E
Published: June 2011

Early thrombosis has complicated human stent implantation in several trials. To determine the best anticoagulation/antiplatelet therapy to maintain stent patency after percutaneous transluminal coronary angioplasty, we implanted the flexible balloon-expandable coil stent into the left anterior descending coronary artery of 28 atherosclerotic 8-month-old Hanford miniature swine. Animals were randomly assigned to one of three treatment groups: group A, aspirin (1 mg/kg/day) and dipyridamole (1 mg/kg three times a day); group B, aspirin and dipyridamole (same doses) plus Coumadin (dose required to prolong prothrombin time 1.3-1.5-fold that of normal); and group C, control. Adjuvant therapy was begun 3 days before stenting. Two pigs (one from group A and one from group B) died during implantation, both without thrombosis. Twenty-six animals survived until follow-up angiography and sacrifice at 1 month. No occlusive thrombosis of the stent occurred in survivors. Reduction of the stent lumen diameter was observed in every case at follow-up. Percent lumen reduction was 19% in group A, 26% in group B, and 24% in group C. Marked smooth muscle cell hyperplasia was seen by light and transmission electron microscopy at stent struts. Scanning electron microscopy of the luminal surface showed a variable morphology consisting of normal endothelium, adherent leukocytes, stellate periluminal cells, and occasional fibrin strands and red blood cells. Luminal narrowing was not affected by anticoagulation therapy, antiplatelet drugs, cholesterol level, or stent sizing. We conclude that occlusive thrombosis does not complicate stent implantation in this model but that substantial luminal narrowing due in part to smooth muscle hyperplasia does occur. The significance of luminal narrowing at the stent site requires further study.
Ischemia-reperfusion impairs endothelium-dependent relaxation of coronary microvessels but does not affect large arteries.
Authors: Quillen J E , Sellke F W , Brooks L A , Harrison D G
Published: June 2011

We examined the effects of ischemia with and without reperfusion on endothelium-dependent and -independent vascular relaxation in both conduit and resistance coronary arteries. Studies were performed on dogs under control conditions (n = 13) or after 1 hour of circumflex coronary artery occlusion with (n = 10) or without (n = 8) 1 hour of reperfusion. Rings of obtuse marginal branches of the left circumflex coronary artery (conduit arteries) were studied in organ chambers. Coronary microvessels (110-220-microns diameter) were studied in a pressurized state with an in vitro microvessel imaging apparatus. Relaxation was evaluated after preconstriction with prostaglandin F2 alpha and U46619 (a thromboxane A2 analogue) in conduit and resistance vessels, respectively. Conduit vessel function was not altered by ischemia with or without reperfusion. Endothelium-dependent microvascular relaxation was depressed in response to acetylcholine, ADP, and calcium ionophore A23187 after ischemia with reperfusion compared with control relaxation (ED50 as -log[M]: 6.0 +/- 0.2 [p less than 0.05], 5.1 +/- 0.4 [p less than 0.05], and 5.8 +/- 0.1 versus 6.8 +/- 0.2, 6.8 +/- 0.2, and 6.6 +/- 0.2, respectively). Ischemia without reperfusion modestly altered microvascular endothelium-dependent relaxation. Microvascular relaxation to nitroglycerin was not altered by ischemia with reperfusion. We conclude that 1) endothelium-dependent relaxation in large epicardial coronary arteries is relatively refractory to ischemia with or without reperfusion, 2) ischemia alone produces mild alterations of coronary microvascular reactivity, 3) ischemia followed by reperfusion produces a marked and selective impairment of endothelium-dependent responses in the coronary microcirculation.
Combined adenosine and lidocaine administration limits myocardial reperfusion injury.
Authors: Homeister J W , Hoff P T , Fletcher D D , Lucchesi B R
Published: June 2011

The endogenous compound adenosine may play a role in limiting myocardial ischemia-reperfusion injury through its ability to cause vasodilation, modulate cardiac adrenergic responses, inhibit neutrophil function, or modulate energy supply and demand of the myocardium. The local anesthetic lidocaine has been shown to be protective against myocardial ischemia-reperfusion injury, although its mechanism of action remains unresolved. We hypothesized that administration of exogenous adenosine during reperfusion would limit the size of the infarct that results from a period of ischemia and reperfusion only when the animals are treated with lidocaine. Male, mongrel dogs (13.0-20.0 kg) were anesthetized (30 mg/kg i.v. sodium pentobarbital), and a left thoracotomy was performed. The left circumflex coronary artery (LCx) was isolated and instrumented with an electromagnetic flow probe, a 25-gauge nonobstructing intracoronary catheter, and a critical stenosis. The dogs were allocated randomly to one of four groups: 1) control, n = 13, (saline), 2) adenosine, n = 13, (0.15 mg/kg/ml/min i.c. for the first hour of reperfusion), 3) lidocaine, n = 9, (2.0 mg/kg i.v. given immediately before coronary artery occlusion and just before reperfusion), or 4) adenosine plus lidocaine, n = 11. The LCx was occluded for 90 minutes and reperfused for 6 hours. Regional myocardial blood flow (RMBF) was determined (n = 6 per group) at 80 minutes of occlusion and at 45 minutes of reperfusion with radiolabeled microspheres. RMBF determinations revealed an increase in blood flow to the inner two thirds of the myocardium at 45 minutes of reperfusion only in the presence of the combined treatment. Adenosine treatment alone or lidocaine treatment alone did not affect RMBF. Quantification of infarct size (triphenyltetrazolium method) expressed as a percent of the area at risk revealed a significant limitation of infarct size only in the group treated with both adenosine and lidocaine: control, 47.8 +/- 6.6%; adenosine, 45.0 +/- 3.2%; lidocaine, 46.9 +/- 6.0%; and adenosine and lidocaine, 20.8 +/- 5.6%. Statistical analyses were performed with two-way analysis of variance to account for the two individual drug treatments. The findings show that intracoronary administration of exogenous adenosine, at the dose used, is only effective at limiting myocardial infarct size when administered to lidocaine-treated animals.
Myocardial catecholamine content after heart transplantation.
Authors: Regitz V , Bossaller C , Strasser R , Schüler S , Hetzer R , Fleck E
Published: June 2011

Myocardial catecholamine levels have not yet been determined in the transplanted human heart. We measured norepinephrine, epinephrine, and dopamine in endomyocardial biopsies from 19 short-term (organ age, 6.6 +/- 6 months) and five long-term (organ age, 62 +/- 2 months) heart transplant patients. Results were compared with those from 10 normal control subjects. In 17 of 19 short-term heart transplant patients, myocardial catecholamines were undetectable, indicating values below 0.1 pg/micrograms noncollagen protein, which was the detection threshold of our assay. In the remaining two patients, myocardial catecholamines (pg/microgram noncollagen protein) were norepinephrine (1.4 and 3.2), epinephrine (0.8 and 1.9), and dopamine (0.9 and 2.3), respectively. In the five long-term heart transplant patients, myocardial catecholamines were not detected. Catecholamine concentrations in 10 healthy control subjects were norepinephrine (10.3 +/- 2.9), epinephrine (0.36 +/- 0.51), and dopamine (0.52 +/- 0.40). Low myocardial norepinephrine levels (less than 20% of control values) with unexplained high levels of epinephrine and dopamine were found in single transplant patients. In most heart transplant patients, however, myocardial catecholamines were undetectable up to five years after transplantation, indicating that the adrenergic response of these hearts probably depends on variations in plasma catecholamines or cardiac beta-receptor density.
Atrial enlargement as a consequence of atrial fibrillation. A prospective echocardiographic study.
Authors: Sanfilippo A J , Abascal V M , Sheehan M , Oertel L B , Harrigan P , Hughes R A , Weyman A E
Published: June 2011

To test the hypothesis that atrial enlargement can develop as a consequence of atrial fibrillation, left and right atrial dimensions were measured echocardiographically at two different time points in patients with atrial fibrillation. Patients were selected who initially had normal atrial sizes and who had no evidence of significant structural or functional cardiac abnormalities other than atrial fibrillation either by history or two-dimensional and Doppler echocardiography. Fifteen patients were studied (12 men and three women; mean age, 67.3 years). Average time between studies was 20.6 months. Three orthogonal left atrial dimensions and two right atrial dimensions were measured, and all were found to increase significantly between studies. Also, highly significant increases in calculated left atrial volume (from 45.2 to 64.1 cm3, p less than 0.001) and right atrial volume (from 49.2 to 66.2 cm3, p less than 0.001) were observed. The relative extents of left and right atrial volume increase did not differ, and left ventricular size did not change significantly between studies. These results indicate that atrial enlargement can occur as a consequence of atrial fibrillation. The maintenance of sinus rhythm, therefore, may prevent atrial enlargement and its adverse clinical effects.
Left ventricular diastolic function. Doppler echocardiographic changes soon after cardiac transplantation.
Authors: StGoar F G , Gibbons R , Schnittger I , Valantine H A , Popp R L
Published: June 2011

In acute cardiac rejection, left ventricular diastolic function is altered, and a restrictive ventricular filling pattern occurs. Doppler echocardiographic indexes of mitral inflow have been proposed as sensitive markers of the rejection process. As rejection progresses, the restrictive ventricular filling pattern is reflected by a shortening of isovolumic relaxation time and mitral valve pressure half-time and by an increase in early transmitral filling velocity. Diastolic function is also compromised in the nonrejecting cardiac transplant recipient during the early postoperative period. This study examined the progression in Doppler-derived mitral filling indexes in 25 recent cardiac transplant recipients who demonstrated no histological evidence of transplant rejection. Isovolumic relaxation time, mitral valve pressure half-time, and early transmitral filling velocity were measured at postoperative weeks 1, 2, 4, and 6 on the day that surveillance right ventricular endomyocardial biopsies were performed. The initial indexes were comparable to previously described restrictive parameters and over the 6-week study period evolved into a nonrestrictive filling pattern. This evolution reflects a progressive improvement in postoperative diastolic function and a decrease in left heart filling pressures. None of the evaluated clinical characteristics, including preoperative pulmonary pressures, total ischemic time of the transplanted heart, cardiopulmonary bypass time, and age of the donor heart, correlated with this process. Given the increasing use of Doppler echocardiography as a means of screening for transplant rejection, it is important to have a thorough understanding of normal postoperative changes in left ventricular diastolic function.
Circadian variation of acute myocardial infarction and the effect of low-dose aspirin in a randomized trial of physicians.
Authors: Ridker P M , Manson J E , Buring J E , Muller J E , Hennekens C H
Published: June 2011

Increased platelet aggregation in the morning and upon assuming an upright posture may account at least in part for the observed circadian variation in onset of acute myocardial infarction. The Physicians' Health Study, a randomized, double-blind, placebo-controlled trial of alternate-day aspirin intake (325 mg) among 22,071 US male physicians, afforded the opportunity to assess this circadian pattern and examine whether it is altered by aspirin therapy. During a 5-year period of follow-up, 342 cases of nonfatal myocardial infarction were confirmed, of which the time of onset was available in 211 (62%). The placebo group showed a bimodal circadian variation in onset of myocardial infarction with a primary peak between 4:00 AM and 10:00 AM (p less than 0.001). In the aspirin group, however, this circadian variation was minimal (p = 0.16), due primarily to a marked reduction in the morning peak of infarction. Specifically, aspirin was associated with a 59.3% reduction in the incidence of infarction during the morning waking hours, compared with a 34.1% reduction for the remaining hours of the day. The greater reduction was observed during the 3-hour interval immediately after awakening, a period with a risk of infarction twice that of any other comparable time interval (p less than 0.001). Aspirin intake was associated with a mean reduction in the incidence of infarction of 44.8% over the entire 24-hour cycle. These data support the hypothesis that increased platelet aggregability in the morning and upon arising contributes to the occurrence of myocardial infarction and that aspirin reduces the risk of infarction by inhibiting platelet aggregation during these critical periods.
Perioperative myocardial infarction after coronary artery bypass surgery. Clinical significance and approach to risk stratification.
Authors: Force T , Hibberd P , Weeks G , Kemper A J , Bloomfield P , Tow D , Josa M , Khuri S , Parisi A F
Published: June 2011

The clinical significance of perioperative myocardial infarction (MI) after coronary artery bypass surgery is not known. Therefore, strategies for the risk stratification of these patients do not exist. This study was undertaken to define the effect of perioperative MI on prognosis after discharge from the hospital and to develop an approach to the risk stratification of these patients. Fifty-nine patients with and 115 patients without perioperative MI were observed for 30 months for the development of cardiac events (death, nonfatal MI, and admission to hospital for unstable angina or congestive heart failure). Patients with perioperative MI were significantly more likely than patients without to have a cardiac event (31% versus 12%, p less than 0.01) and multiple events (19% versus 1%, p less than 0.001). Cox regression analysis identified two independent predictors of cardiac events other than perioperative MI (relative risk, 2.7): inadequate revascularization (relative risk, 3.5) and depressed (less than 40%) postoperative ejection fraction (EF) (relative risk, 2.1). Event-free survival rate of patients with perioperative MI varied markedly depending on the number of other negative prognostic variables present. Patients with perioperative MI who were adequately revascularized and had a postoperative EF greater than 40% had an event-free survival rate similar to patients without a perioperative MI (92% versus 87%, p = NS). Patients with perioperative MI who were inadequately revascularized and had depressed postoperative EF had an event-free survival rate of 13% (p less than 0.001 versus all other subsets). Event-free survival rate was intermediate (68%) in patients with perioperative MI and with only one of the other two variables (p less than 0.001 versus other subsets). In conclusion, perioperative MI adversely affects prognosis. Patients can be stratified into low, high, and intermediate risk subsets based on a simple assessment of the adequacy of revascularization and a determination of residual left ventricular function.
Reversal of segmental hypokinesis by coronary angioplasty in patients with unstable angina, persistent T wave inversion, and left anterior descending coronary artery stenosis. Additional evidence for myocardial stunning in humans.
Authors: Renkin J , Wijns W , Ladha Z , Col J
Published: June 2011

To evaluate the significance of persistent negative T waves during severe ischemia, we prospectively studied 62 patients admitted for unstable angina without evidence of recent or ongoing myocardial infarction. A critical stenosis on the left anterior descending coronary artery (LAD), considered as the culprit lesion, was successfully treated by percutaneous transluminal coronary angioplasty (PTCA). The patients were divided into two groups according to the admission electrocardiogram: T NEG group (n = 32) had persistent negative T waves, and the T POS group (n = 30) had normal positive T waves on precordial leads. The two groups had similar baseline clinical, hemodynamic, and angiographic characteristics. All patients underwent a complete clinical and angiographic evaluation (coronary arteriography and left ventriculography) before undergoing PTCA and 8 +/- 3 months later. Left ventricular anterior wall motion was evaluated by the percent shortening of three areas (S1, S2, and S3) considered as LAD-related segments on left ventriculograms. Before PTCA, there was no significant difference in global ejection fraction between the two groups despite a significant depression in anterior mean percent area shortening in the T NEG compared with the T POS group (S1, 44 versus 54, p less than 0.01; S2, 39 versus 48, p less than 0.01; S3, 44 versus 50, NS). At repeated angiography, the anterior mean percent area shortening improved significantly in the T NEG group (S1, from 44 to 61, p less than 0.001; S2, from 39 to 58, p less than 0.001; S3, from 44 to 61, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
Ventricular refractory period extension caused by defibrillation shocks.
Authors: Sweeney R J , Gill R M , Steinberg M I , Reid P R
Published: June 2011

In pentobarbital-anesthetized dogs, transcardiac shocks of up to 30 J or pacing stimuli were delivered to myocardial tissue at different times in the electrical cycle. When delivered midway or later into electrical systole, shocks, but not pacing stimuli, greatly extended the refractory period as determined by left ventricular pacing. There was a positive correlation between both the shock energy and timing and the amount of delay. A 30-J shock given 10 msec before the end of the refractory period extended the refractory period by 63 +/- 15 msec (p less than 0.001), whereas the same shock given 40 msec earlier produced only 25 +/- 10 msec (p less than 0.001) of extension. By comparison, a 5-J shock given at those times produced 36 +/- 18 (p less than 0.005) and 10 +/- 8 msec (p less than 0.001) of extension, respectively. When delivered early into electrical systole, both a pacing stimulus and a shock had no substantial effect on the tissue refractory period. Because the tissue that is late in electrical systole would otherwise be the first to repolarize if no shock were given, the selective refractory period extension may create a period after the shock during which no tissue is repolarized to a level sufficient for wavefront propagation. Thus, the energy- and time-dependent refractory period extension may help explain the mechanism by which ventricular defibrillation occurs during transcardiac shocks.
Estimation of mean left atrial pressure from transesophageal pulsed Doppler echocardiography of pulmonary venous flow.
Authors: Kuecherer H F , Muhiudeen I A , Kusumoto F M , Lee E , Moulinier L E , Cahalan M K , Schiller N B
Published: June 2011

To determine whether pulmonary venous flow and mitral inflow measured by transesophageal pulsed Doppler echocardiography can be used to estimate mean left atrial pressure (LAP), we prospectively studied 47 consecutive patients undergoing cardiovascular surgery. We correlated Doppler variables of pulmonary venous flow and mitral inflow with simultaneously obtained mean LAP and changes in pressure measured by left atrial or pulmonary artery catheters. Among the pulmonary venous flow variables, the systolic fraction (i.e., the systolic velocity-time integral expressed as a fraction of the sum of systolic and early diastolic velocity-time integrals) correlated most strongly with mean LAP (r = -0.88). Of the mitral inflow variables, the ratio of peak early diastolic to peak late diastolic mitral flow velocity correlated most strongly with mean LAP (r = 0.43), but this correlation was not as strong as that with the systolic fraction of pulmonary venous flow. Similarly, changes in the systolic fraction correlated more strongly with changes in mean LAP (r = -0.78) than did changes in the ratio of peak early diastolic to peak late diastolic mitral inflow velocity (r = 0.68). We conclude that in the surgical setting observed, pulmonary venous flow from transesophageal pulsed Doppler echocardiography can be used to estimate mean LAP. This technique may provide a rapid, simple, and relatively noninvasive means of gauging this variable in patients undergoing intraoperative transesophageal echocardiography.
Top-resolution frequency analysis of electrocardiogram with adaptive frequency determination. Identification of late potentials in patients with coronary artery disease.
Authors: Haberl R , Schels H F , Steinbigler P , Jilge G , Steinbeck G
Published: June 2011

Frequency analysis of the electrocardiogram with Fourier transform is a sensitive method of detecting late potentials. However, information about localization of late potentials is lost, frequency resolution is poor, and window functions have to be applied. We therefore analyzed multiple segments (25 msec long) of the surface electrocardiogram ("spectrotemporal mapping") with adaptive frequency determination (AFD), an autoregressive algorithm that is characterized by high-frequency resolution in very short segments without the use of window functions. Results were compared with those from Fourier transform and the Simson method. We studied 38 patients after myocardial infarction (MI) with sustained ventricular tachycardia (VT), 21 patients after MI without VT, and 18 healthy subjects. Frequency peaks could be clearly differentiated until a minimal interval of 6 Hz; with fast Fourier transform (Blackman Harris window) in a much longer segment (80 msec), the spectral peaks merged into one another at an interval of about 30 Hz. AFD revealed high-frequency components as narrow peaks in the range of 40-160 Hz in 28 of 38 patients (74%) after MI with VT. Because of the short segment size, exact localization of late potentials was possible; in most of the patients, the peaks occurred in segments inside the QRS complex and ended 20 +/- 10 msec after termination of the QRS complex. In patients after MI without VT, only four of 21 patients (19%) had spectral peaks in segments after the end of the QRS complex; however, 13 of 21 patients demonstrated microvolt potentials in segments within the QRS complex. These potentials did not extend beyond the end of normal ventricular activation. Only two of 18 healthy subjects showed abnormal AFD results. Patients with bundle branch block did not need to be excluded. AFD allowed good differentiation between late potentials and noise by a characteristic pattern of the spectral peaks. For the Simson method, patients with bundle branch block had to be excluded, and overall sensitivity was 42%. In five cases, the cause of failure of the Simson method could be identified as incorrect determination of the QRS limits due to noise. Thus, AFD is a promising method for detailed analysis of late potentials; it combines the advantages of frequency analysis (good differentiation between signal and noise and high-pass filters not necessary) and time domain analysis (localization of late potentials).
Evaluation of the associations between carotid artery atherosclerosis and coronary artery stenosis. A case-control study.
Authors: Craven T E , Ryu J E , Espeland M A , Kahl F R , McKinney W M , Toole J F , McMahan M R , Thompson C J , Heiss G , Crouse J R
Published: June 2011

To evaluate the consistency, strength, and independence of the relation of carotid atherosclerosis to coronary atherosclerosis, we quantified coronary artery disease risk factors and extent of carotid atherosclerosis (B-mode score) in 343 coronary artery disease patients and 167 disease-free control patients. In univariable analyses, there was a strong association between coronary status and extent of carotid artery disease in men and women older than and younger than 50 years (p less than 0.001 for men and women greater than 50 years, p less than 0.001 for women less than or equal to 50 years, p = 0.045 for men less than or equal to 50). The relation remained strong after control for age in men and women older than 50 years and in women younger than 50 (p less than 0.001 for men and women greater than 50 years, p = 0.003 for women less than or equal to 50) but did not persist after control for age in men younger than 50. Logistic models that included coronary disease risk factors, with or without B-mode score, as independent variables and presence or absence of coronary disease as the outcome variable indicated that the extent of carotid atherosclerosis was a strong, statistically significant independent variable in models for men and women older than 50 years of age. Next, we examined the usefulness of B-mode score as an aid in screening for coronary artery disease in men and women older than 50 years. Classification rules, both including and excluding B-mode score, were developed based on logistic regression and, for comparison, recursive partitioning (decision trees). The performance of these rules and the bias of their performance statistics were estimated. The improved classification of the study sample when B-mode score was incorporated in the rule was statistically significant only for men (p = 0.015). However, the addition of B-mode score was found to 1) increase the median discrimination score for both sex groups based on the logistic model, and 2) yield better sensitivities and specificities for rules based on recursive partitioning. Thus B-mode score is strongly, consistently, and independently associated with coronary artery disease in patients older than 50 and is at least as useful as well-known risk factors for identifying patients with coronary artery disease.
Determinants of cardiac involvement in children and adolescents with essential hypertension.
Authors: Daniels S D , Meyer R A , Loggie J M
Published: June 2011

Left ventricular hypertrophy is often found in association with systemic hypertension and may be an independent risk factor for cardiovascular disease morbidity and mortality. Few studies have investigated the determinants of left ventricular mass (LVM) in young patients with essential hypertension. Therefore, we studied 104 children and adolescents with blood pressure persistently greater than the 90th percentile for age and sex and with no known cause of blood pressure elevation. LVM was determined by echocardiography and was indexed by height to account for body size. The mean LVM index was 90.2 +/- 26.0 g/m. Using the gender-specific 95th percentile from normal children, 40 subjects (38.5%) had left ventricular hypertrophy. Using multiple regression analysis, the significant independent direct correlates of LVM index were male sex, body mass index, dietary sodium intake, age at diagnosis, and systolic blood pressure at maximum exercise. The significant independent inverse correlate of LVM index was resting heart rate (p less than 0.05). These variables accounted for a substantial portion of the LVM index variance in this population (multiple R2 = 0.56, p less than 0.001). The results indicate that left ventricular hypertrophy is prevalent in children and adolescents with essential hypertension. The direct association of LVM index with body mass index and dietary sodium intake suggests weight reduction and dietary salt restriction might be useful to prevent or treat the development of left ventricular hypertrophy in pediatric patients with essential hypertension.
Increase of Gi alpha in human hearts with dilated but not ischemic cardiomyopathy.
Authors: Böhm M , Gierschik P , Jakobs K H , Pieske B , Schnabel P , Ungerer M , Erdmann E
Published: June 2011

In myocardial membranes from hearts with dilated cardiomyopathy (DCM), there was a 37% increase of the Gi alpha-protein as measured by 32P-ADP-ribosylation of a approximately 40 kDa pertussis toxin substrate. Immunoblotting techniques also showed increased amounts of Gi alpha in DCM. In hearts with ischemic cardiomyopathy (ICM), Gi alpha was not altered compared with nonfailing myocardium (NF). Basal and Gpp(NH)p-stimulated adenylate cyclase activity was reduced in DCM but not in ICM. The number of beta-adrenoceptors was similarly reduced both in DCM and ICM compared with NF. Alterations of m-cholinoceptors or A1-adenosine receptors did not occur. Consistently, "indirect" negative inotropic effects of the m-cholinoceptor agonist carbachol and the A1-adenosine receptor agonist R-PIA were not different in ICM, DCM, and nonfailing myocardium. In ICM and DCM, there was a marked reduction of the positive inotropic responses to isoprenaline and milrinone. However, there was a further reduction in DCM compared with ICM. It is concluded that the increase of Gi alpha is accompanied by a reduction of basal and guanine-nucleotide-stimulated adenylate cyclase activity. Alterations of m-cholinoceptors and A1-adenosine receptors do not appear to be involved. The further decrease of the positive inotropic effects of isoprenaline and milrinone in DCM provides evidence that the increase of Gi alpha is functionally relevant in DCM but not ICM and hence might contribute to the reduced effects of endogenous catecholamines and exogenous cAMP-dependent positive inotropic agents in the former but not the latter condition.
Noninvasive quantification of regional myocardial perfusion with rubidium-82 and positron emission tomography. Exploration of a mathematical model.
Authors: Herrero P , Markham J , Shelton M E , Weinheimer C J , Bergmann S R
Published: June 2011

Positron emission tomography (PET) centers without cyclotrons use generator-produced rubidium-82 (82Rb) for assessment of myocardial perfusion. The aim of the present study was to determine whether myocardial blood flow could be assessed quantitatively with 82Rb and PET. Because the myocardial extraction fraction of 82Rb varies inversely and nonlinearly with flow and cannot be measured conveniently with PET, we used an experimentally derived mathematical function defining the relation between single-pass extraction fraction of 82Rb and flow to obviate the necessity of measuring the extraction fraction directly. Myocardial blood flow in absolute terms (ml/g/min) was estimated from dynamic PET scans after intravenous administration of 82Rb in intact dogs and compared with flows measured with radiolabeled microspheres. In 36 comparisons in 13 dogs studied at rest, or after coronary occlusion, reperfusion, or after coronary hyperemia induced with intravenous dipyridamole, over the flow range from 0.2 to 2.0 ml/g/min, estimates of perfusion with rubidium correlated well with flows measured concomitantly with microspheres, although there was a slight underestimation of flow with rubidium (flow by 82Rb = 0.92 x flow by microspheres-0.021, r = 0.83). In general, estimates of flow in ischemic regions were less reliable than estimates for regions with normal flow. Thus, although the relation between myocardial extraction and retention of 82Rb and flow can vary under a variety of physiological and pathophysiological conditions, this study demonstrates the ability to obtain quantitative estimates of myocardial blood flow with 82Rb and PET under carefully defined conditions without measuring the extraction fraction directly.
Time course of endothelial dysfunction and myocardial injury during myocardial ischemia and reperfusion in the cat.
Authors: Tsao P S , Aoki N , Lefer D J , Johnson G , Lefer A M
Published: June 2011

Myocardial ischemia and reperfusion have been shown to impair coronary vasorelaxation to endothelium-dependent vasodilators. To examine the time course of this dysfunction, occlusion of the left anterior descending (LAD) coronary artery (90 minutes) was followed by reperfusion for 0, 2.5, 5, 20, 180, or 270 minutes. Coronary arterial rings from the ischemic LAD and control left circumflex (LCx) arteries were tested for responsiveness to the endothelium-dependent receptor-mediated vasodilator, acetylcholine (ACh), and the endothelium-dependent nonreceptor-mediated vasodilator, A23187, as well as the endothelium-independent vasodilator, NaNO2. ACh relaxation was not impaired after 90 minutes of ischemia without reperfusion. However, 2.5 minutes of reperfusion resulted in depressed ACh responses (36 +/- 10% of control) that was further reduced to 16 +/- 6% at 20 minutes, and remained comparably depressed at every time thereafter. A23187 vasodilator responses were also attenuated after reperfusion, although the reduced response occurred later (that is, at 20 minutes). There was no significant decrease in response to NaNO2 in the LAD at any time or to any vasodilator in LCx control rings. Treatment with recombinant human superoxide dismutase (hSOD, 5 mg/kg/hr, that is, 15,545 SOD units/kg/hr), starting 10 minutes before reperfusion, preserved the vasodilator response to ACh (82 +/- 6%) and A23187, but treatment with the hydroxyl ion scavenger N-(2-mercapto proprionyl)-glycine (MPG) (8 mg/kg/hr) only protected the A23187 response. No damage to the surface of the endothelium was observed by scanning electron microscopy at any time point. Myocardial cell damage increased with time of reperfusion as assessed by increasing plasma CK activities and amounts of necrotic tissue indexed to area at risk. Significant myocardial injury occurred at 3 hours after reperfusion. These findings suggest that endothelial dysfunction resulting in reduced endothelium-derived relaxing factor release occurs before the development of myocardial cell necrosis and may be due to oxygen-derived free radicals produced rapidly on reperfusion.
Characterization of regional diastolic pressure gradients in the right ventricle.
Authors: Courtois M , Barzilai B , Gutierrez F , Ludbrook P A
Published: June 2011

Regional intraventricular pressure gradients exist in the left ventricle (LV) during both the early and late filling phases of diastole. These regional pressure gradients comprise a fundamental component of the mechanism of normal LV filling. To determine whether similar diastolic pressure gradients also occur in the right ventricle (RV), we measured right atrial (RA) and RV regional pressures with use of micromanometers in six anesthetized, closed-chest dogs. Tricuspid flow velocity was recorded with use of transesophageal Doppler echocardiography, and right ventriculograms were obtained with contrast angiography. As in the LV, the maximum RA-RV pressure gradient during early diastole was consistently greater if RV pressure was measured near the apex than in the inflow tract (1.6 +/- 0.5 versus 0.8 +/- 0.4 mm Hg). The area of reversed pressure was also found to be significantly greater in the apex than in the inflow tract (72 +/- 43 versus 8 +/- 6 mm Hg.msec). However, unlike the LV, the lowest minimum pressure was usually recorded in the RV outflow tract, resulting in a significantly increased RA-RV outflow tract pressure gradient compared with the RA-RV apex pressure gradient (2.5 +/- 0.8 versus 1.6 +/- 0.5 mm Hg). Analysis of right ventriculograms indicates marked narrowing of the RV outflow tract at end systole in all six animals, suggesting that an end-systolic deformation in this region is the likely mechanism for production of low early diastolic pressure in this region. During atrial contraction the RV regional pressure gradient pattern was similar to the LV pattern: the RV a-wave ascent occurred earlier in the inflow tract and later in the apex. A-wave ascent appeared to occur almost simultaneously in the apex and outflow tract. In the six animals, Doppler-derived peak tricuspid flow velocity during early diastole was 35 +/- 6 cm/sec. Early tricuspid flow acceleration (393 +/- 101 cm/sec2) was found to be significantly greater than deceleration of flow (182 +/- 59 cm/sec2). Comparison of tricuspid pressure-flow data with mitral pressure-flow data previously obtained in our laboratory indicates that the driving pressure gradient across the tricuspid valve is significantly less than across the mitral. This pressure difference corresponds to differences in acceleration and peak flow found across the two valves. Consideration of these physiological patterns of RV diastolic intraventricular pressure and their relation to filling has important implications with regard to the development of indexes that characterize diastolic pressure-flow relations and provides physiological insight relating to the location of ventricular restoring forces.
Hirudin, heparin, and placebo during deep arterial injury in the pig. The in vivo role of thrombin in platelet-mediated thrombosis.
Authors: Heras M , Chesebro J H , Webster M W , Mruk J S , Grill D E , Penny W J , Bowie E J , Badimon L , Fuster V
Published: June 2011

Three dosages (0.3, 0.7, and 1.0 mg/kg) of recombinant hirudin, a specific inhibitor of thrombin, were compared with heparin (50 units/kg) and placebo for reducing thrombus formation in the carotid arteries of 50 pigs after deep injury by balloon dilatation. Each drug was administered as a bolus followed immediately by a continuous infusion of the same dose per hour. Major end points were quantitative indium-111-labeled platelet and iodine-125-labeled fibrinogen deposition and the incidence of mural thrombosis. This study showed that heparin, at a dose that prolonged the activated partial thromboplastin time (APTT) to twice the control time, did not prevent mural thrombosis or significantly reduce platelet deposition compared with placebo but did reduce fibrinogen deposition. Recombinant hirudin markedly reduced platelet and fibrinogen deposition in a dose-related manner and totally eliminated mural thrombosis at an APTT of two to three times that of control. Platelet deposition (x 10(6)/cm2, mean +/- SEM) in areas of deep arterial injury for the placebo, heparin, and 0.3, 0.7, and 1.0 mg/kg hirudin groups was 54 +/- 21, 33 +/- 9, 22 +/- 6, 8 +/- 1, and 7 +/- 1, respectively; electron microscopy showed a single layer (or less) of platelets at the two highest hirudin dosages. The incidence of macroscopic mural thrombosis was 76% with placebo, 57% with heparin, 46% with 0.3 mg/kg hirudin; there were no thrombi with 0.7 or 1.0 mg/kg hirudin (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)