Evaluation of two different rapid maxillary expansion surgical techniques and their effects on the malar complex based on 3d cone-beam computed tomography.

We compared and evaluated the effects of two techniques used for surgically assisted rapid maxillary expansion (SARME) using three-dimensional (3D) cone-beam computed tomography, focusing on changes in soft and hard tissue in the malar region. A conventional Le Fort I osteotomy group (10 patients, mean age: 19.3 years) and a high Le Fort I group (12 patients, mean age: 20.4 years) underwent 3D analyses. Changes in hard and soft tissue of the malar region were compared. The average increases in the bone malar width and soft malar width in the high Le Fort I group between the pre- and postoperative periods were 1.43 ± 1.23 and 1.39 ± 1.19 mm, respectively. The average increases in the bone malar depth on the right and left sides in the high Le Fort I group were 1.34 ± 0.81 and 1.60 ± 0.54 mm, respectively. Progress in hard tissues did not reflect significant changes in soft tissue. CONTEXT: Effects of high Le Fort I SARME on the malar complex. AIMS: To compare and evaluate the effects of two techniques used for SARME, using 3D cone-beam computed tomography, focusing on changes in hard and soft tissues in the malar region. SETTINGS AND DESIGN: A conventional Le Fort I osteotomy group (10 patients, mean age: 19.3 years) and a high Le Fort I group (12 patients, mean age: 20.4 years). METHODS AND MATERIAL: Each group underwent 3D analyses, and changes in hard and soft tissues of the malar region were compared. STATISTICAL ANALYSIS USED: The SPSS software (ver. 15.0 for Windows) was used. The Kolmogorov-Smirnov test, Student's t test, and paired-samples test were conducted. RESULTS: The average increases in the bone malar width and soft malar width in the high Le Fort I group between the pre- and postoperative periods were 1.43 ± 1.23 and 1.39 ± 1.19 mm, respectively. The average increases in the bone malar depth on the right and left sides in the high Le Fort I group were 1.34 ± 0.81 and 1.60 ± 0.54 mm, respectively. CONCLUSIONS: Progress in hard tissues did not reflect significant changes in soft tissue.

Volumetric changes of the upper airway following maxillary and mandibular advancement using cone beam computed tomography.

The objective of this project was to retrospectively evaluate changes in volume of different compartments of the upper airway in response to maxillary, mandibular, and bimaxillary advancement surgeries and to predict the extent of volumetric changes associated with these surgical movements. Pre- and post-surgical cone beam computed tomography scans of 36 patients were evaluated for changes in nasal cavity, nasopharyngeal, oropharyngeal, and hypopharyngeal compartments. The amount of movement for each surgery was measured from skeletal landmarks to reference planes and was correlated with volumetric changes. Maxillary advancement of 4.0±2.2mm increased the oropharyngeal volume significantly (41.40%), and mandibular advancement of 3.8±1.6mm also significantly increased the oropharyngeal volume (21.17%). Bimaxillary advancement of 5.1±1.3mm for the maxilla and 6.4±3.1mm for the mandible significantly increased nasopharyngeal (27.45%), oropharyngeal (66.39%), and hypopharyngeal (52.48%) volumes. Furthermore, for every millimeter anterior movement, oropharyngeal volume increased by 2319.2±771.8mm3. Bimaxillary advancement showed a greater increase than isolated maxillary and mandibular advancement in all pharyngeal compartments. Every millimeter of advancement in the bimaxillary group led to a significant increase in oropharyngeal volume, while every millimeter downward movement showed a significant increase in nasopharyngeal volume.

Shortened Doppler-derived mitral A wave deceleration time: an important predictor of elevated left ventricular filling pressure.

OBJECTIVES: The aim of this study was to investigate whether a new variable of mitral inflow, A wave deceleration time, identifies patients with elevated left ventricular filling pressures. BACKGROUND: In patients with an elevated left ventricular end-diastolic pressure, the increase in left ventricular pressure after atrial contraction rapidly exceeds left atrial pressure, resulting in abrupt cessation of the A wave. Therefore, we postulated that a shortening of A wave deceleration time might be a marker for elevated end-diastolic pressure. METHODS: Adequate pulsed Doppler mitral inflow velocities could be recorded in 40 of 44 consecutive patients undergoing cardiac catheterization with capillary wedge pressure in 20 patients, and within 1 h after left ventricular end-diastolic pressure recording in 20. Fifteen healthy volunteers were also studied. RESULTS: Left ventricular end-diastolic pressure was 8 to 35 mm Hg, and mean pulmonary wedge pressure was 6 to 37 mm Hg. Close correlations were found between A wave deceleration time and mean pulmonary wedge pressure (r = -0.87) and left ventricular end-diastolic pressure (r = -0.74). There were modest correlations between both pressures and peak E/A, E wave deceleration time and A wave duration, respectively; r = 0.59, -0.30 and -0.58 for capillary wedge and r = 0.25, -0.38 and -0.49 for end-diastolic pressures. A wave deceleration time 18 mm Hg, respectively, with a sensitivity of 67% and 89% and specificity of 100% for both. CONCLUSIONS: A shortened Doppler mitral inflow A wave deceleration time is a useful index of elevated left ventricular filling pressure.

Effect of thrombolytic therapy on the evolution of significant mitral regurgitation in patients with a first inferior myocardial infarction.

OBJECTIVES: This study was designed to test the hypothesis that reperfusion therapy with thrombolysis will prevent the development of significant mitral regurgitation in patients with inferior myocardial infarction. BACKGROUND: The value of thrombolytic therapy in patients with inferior or posterior wall myocardial infarction has been controversial. We hypothesized that successful reperfusion therapy with intravenous thrombolysis may reduce the incidence and severity of postinfarction mitral regurgitation in this patient group. METHODS: We prospectively studied 104 patients with a first inferior myocardial infarction. Thrombolytic therapy was administered to 55 patients (treatment group) 3.2 +/- 2.1 h after the onset of symptoms. The other 49 patients formed the control group. Doppler echocardiographic color flow imaging was performed in all patients within 24 h, at 7 to 10 days and at 28 to 30 days after myocardial infarction. Significant mitral regurgitation was defined as moderate or severe (grade 2 or 3). RESULTS: No significant differences in baseline clinical characteristics were observed between the treatment and control groups. The overall incidence rates of significant mitral regurgitation at 24 h, 7 to 10 days and at 28 to 30 days were 10 (10%) of 104 patients, 18 (17%) of 104 patients and 11 (11%) of 100 patients, respectively. Multivariate analysis reveals the following independent predictors of the occurrence of significant mitral regurgitation: female gender (at 7 to 10 days, odds ratio 5.3, 90% confidence interval [CI] 1.8 to 15.5; at 28 to 30 days, odds ratio 3.7, 90% CI 1.1 to 12.7), heart failure (at 7 to 10 days, odds ratio 7.7, 90% CI 2.2 to 26.9) and transient complete atrioventricular block (at 24 h of myocardial infarction, odds ratio 5.8, 90% CI 1.2 to 27). Compared with the control group, the treatment group exhibited marked reduction in the incidence of significant mitral regurgitation at 24 h (16% vs. 4%; odds ratio 0.1, 90% CI 0.0 to 0.7); at 7 to 10 days (24% vs. 11%; odds ratio 0.3, 90% CI 0.1 to 0.9) and at 28 to 30 days (15% vs. 7%; odds ratio 0.4, 90% CI 0.1 to 1.6). Severe (grade 3) mitral regurgitation developed in five patients in the control group but in no patient in the treatment group. CONCLUSIONS: Thrombolytic therapy in the patients with a first inferior myocardial infarction was associated with a reduced incidence of significant mitral regurgitation. These results support the use of such therapy in patients with inferior myocardial infarction.

Additional ST segment elevation during the first hour of thrombolytic therapy: an electrocardiographic sign predicting a favorable clinical outcome.

OBJECTIVES: The aim of this study was to investigate the significance of further ST elevation that occurs during the 1st h of thrombolytic therapy before the expected resolution. BACKGROUND: Early resolution of ST segment elevation is commonly accepted as a marker of clinical reperfusion during thrombolytic therapy for acute myocardial infarction. Using frequent electrocardiographic recordings, we observed in some patients further ST elevation that occurred during hour 1 of thrombolysis before the expected resolution. METHODS: To investigate the significance of this pattern, we classified 177 consecutive patients with a first acute myocardial infarction into two groups: Group A, 98 patients with ST elevation > or = 1 mm above the initial ST elevation during the 1st h of thrombolytic therapy, and Group B, 79 patients without this finding. RESULTS: Although the presence or absence of additional ST elevation was not associated with a clinical or prognostic difference in patients with a first inferior or posterior acute myocardial infarction, its presence indicated a more favorable clinical outcome and prognosis in patients with anterior infarction. Among the patients with anterior infarction the 65 patients in Group A had a higher ejection fraction (44 +/- 9% vs. 35 +/- 11%, p < 0.01), less heart failure (15% vs. 35%, p = 0.02) and a lower in-hospital mortality rate (0% vs. 8%, p = 0.04) than did the 37 patients from Group B. CONCLUSIONS: Additional ST elevation early during thrombolytic therapy in patients with anterior infarction suggests a favorable clinical outcome and thus may be indicative of successful reperfusion.

Improved posterobasal segment function after thrombolysis is associated with decreased incidence of significant mitral regurgitation in a first inferior myocardial infarction.

OBJECTIVES: This study was designed to investigate the association between wall motion abnormalities and the occurrence of ischemic mitral regurgitation in patients with a first inferior or posterior myocardial infarction and to reassess the role of thrombolytic treatment in these patients. BACKGROUND: We previously demonstrated that thrombolytic therapy reduces the incidence of significant mitral regurgitation in patients with a first inferior myocardial infarction, but the mechanisms responsible for this decrease were not clear. METHODS: Wall motion score on two-dimensional echocardiography (16 segments) and mitral regurgitation grade (0 to 3) on Doppler color flow imaging were assessed in 95 patients (in 47 after thrombolysis) at 24 h, 7 to 10 days and 1 month after myocardial infarction. Significant mitral regurgitation was defined as moderate or severe (grade 2 or 3). RESULTS: Multivariate analysis revealed that the presence of an advanced wall motion abnormality of the posterobasal segment of the left ventricle was the most significant independent variable associated with significant mitral regurgitation: odds ratio (OR) 15.0, 90% confidence interval (CI) 1.4 to 165.6 at 24 h; OR 2.8, CI 0.9 to 9.3 at 7 to 10 days; OR 4.2, CI 1.2 to 11.4 at 1 month. Thrombolysis reduced the prevalence of advanced wall motion abnormalities in the posterobasal segment at 24 h (55% vs. 75%, OR 0.5, CI 0.2 to 0.99), 7 to 10 days (44% vs. 73%, OR 0.3, CI 0.1 to 0.7) and 1 month (36% vs. 56%, OR 0.4, CI 0.2 to 0.9). CONCLUSIONS: There is a strong association between advanced wall motion abnormalities in the posterobasal segment and significant mitral regurgitation. In this study group, thrombolysis reduced the prevalence of advanced wall motion abnormalities in the posterobasal segment and thereby reduced the incidence of significant mitral regurgitation.

Left ventricular pseudohypertrophy in cardiac tamponade: an echocardiographic study in a canine model.

OBJECTIVES: This study was designed to establish whether left ventricular pseudohypertrophy in cardiac tamponade can be reproducibly induced in an experimental canine model and to investigate the mechanism of its production. BACKGROUND: Past experimental and clinical studies have shown reduction of ventricular volumes resulting from cardiac tamponade. Left ventricular pseudohypertrophy, a transient thickening of myocardial walls, was recently described as a new echocardiographic sign of cardiac tamponade. METHODS: Cardiac tamponade was induced in seven anesthetized open chest dogs with serial bolus injections of 50 ml each of 0.9% saline solution into the pericardial sac. Under hemodynamic monitoring, M-mode and two-dimensional echocardiographic measurements were performed from a right parasternal window at each stage of graded cardiac tamponade. RESULTS: There was a progressive increase of interventricular septal and posterior wall diastolic thickness. Mean wall thickness (interventricular septal thickness + posterior wall thickness divided by 2) was 9.8 +/- 1.3 mm at baseline, 14.3 +/- 0.9 mm at peak tamponade and 9.0 +/- 1.5 mm after fluid withdrawal (p < 0.0001). Mean wall thickness correlated directly with the severity of cardiac tamponade, as estimated from the level of right arterial pressures (r = 0.75 and p < 0.0001), and with the decrease of left ventricular cavity volume (r = -0.67 and p < 0.0001). Left ventricular mass did not change significantly. CONCLUSIONS: Left ventricular pseudohypertrophy is a constant manifestation of cardiac tamponade in a canine model. The degree of myocardial thickening correlates with the reduction of ventricular dimensions and with the severity of hemodynamic compromise, representing a constant facet of heart remodeling in cardiac tamponade.

Unusual pericardial calcification in Gaucher's disease.

Gaucher's disease is a hereditary metabolic disorder characterized by the abnormal accumulation of glucocerebrosides in reticuloendothelial cells. A 58-year-old man had Gaucher's disease and suffered from hypersplenism, cirrhosis of the liver, and free-floating calcifications in the pericardial space. The literature of the pericardial involvement in Gaucher's disease is reviewed.

Hypertension in diet versus pharmacologically treated diabetics: mortality over a 5-year follow-up.

The natural history of non-insulin-dependent diabetes mellitus (NIDDM) differs markedly between patients with diet treated and pharmacologically treated disease. However, the interrelationship between hypertension and these common diabetes types has not been specifically addressed in previous studies. This study was designed to evaluate the prognostic significance and prevalence of hypertension in coronary patients with diet versus pharmacologically treated NIDDM over a 5-year follow-up period. The study sample comprised 11 515 patients aged 45 to 74 years with a previous myocardial infarction and/or anginal syndrome who had been screened but were not included in the Bezafibrate Infarction Prevention study. Among them, 9033 were nondiabetics and 2482, diabetics (987 diet treated and 1495 pharmacologically treated). The prevalence of hypertension among nondiabetics, diet-treated diabetics, and pharmacologically treated diabetics was 31%, 42%, and 43%, respectively. Crude all-cause mortality (CM) was lower in the nondiabetic patients (11.2% versus 22.0%; P<0.001). Among diabetics, 548 patients died: 81 diet treated normotensives (CM 14%); 100 diet-treated hypertensives (CM 24.4%); 205 pharmacologically treated normotensives (CM 24.2%); and 162 pharmacologically treated hypertensive patients (CM 25.0%). Age-adjusted mortality was lowest for the normotensive patients in the diet-treated group and highest for the hypertensive pharmacologically treated patients. Multivariate analysis shows that hypertension is a strong and independent predictor of increased CM in diet-treated but not in pharmacologically treated NIDDM: hazard ratio (HR) was 1.68 (95% confidence interval [CI] 1.24 to 2.29) for the diet-treated versus 1. 01 (95% CI 0.82 to 1.26) for the pharmacologically treated diabetics. The contribution of hypertension to stroke mortality was substantial for both diet treated and pharmacologically treated NIDDM: hazard ratios were 3.17 (95% CI 1.12 to 8.98) and 2.21 (95% CI 0.72 to 6.77), respectively. The increased risk of mortality associated with hypertension in relatively mild diet-treated NIDDM strongly supports the clinical benefit of early blood pressure control among diabetic patients with ischemic heart disease.

Thiamine deficiency in patients with congestive heart failure receiving long-term furosemide therapy: a pilot study.

PURPOSE: To test the hypothesis that long-term furosemide therapy in patients with congestive heart failure (CHF) is associated with clinically significant thiamine deficiency via urinary loss. DESIGN: (1) Biochemical evaluation of thiamine status in hospitalized patients with CHF treated with long-term furosemide and in age-matched control patients. (2) Uncontrolled trial of the effect of intravenous thiamine on cardiac performance in a subset of six patients with CHF. SETTING: General medical ward of a teaching community hospital. PATIENTS: Twenty-three patients with chronic CHF receiving furosemide, and 16 age-matched control patients without heart failure and not taking diuretics. Daily furosemide doses were 80 to 240 mg, and duration of furosemide therapy was 3 to 14 months. Patients with identifiable causes of inadequate thiamine intake, absorption, or utilization or increased metabolic requirements were excluded. INTERVENTION: A 7-day course of intravenous thiamine, 100 mg twice daily, in six consenting patients with CHF. RESULTS: A high thiamine pyrophosphate effect (TPPE), indicating thiamine deficiency, was found in 21 of 23 furosemide-treated patients and in two of 16 controls (p less than 0.001). The mean (+/- SE) TPPE (normal: 0% to 15%) in furosemide-treated and control patients was 27.7 +/- 2.5% and 7.1 +/- 1.6%, respectively (p less than 0.001). Despite the high TPPE, the mean (+/- SE) urinary thiamine excretion in the furosemide-treated patients (n = 18) was inappropriately high (defined as greater than 130 micrograms/g creatinine), 410 +/- 95 micrograms/g creatinine, even in comparison with that in the controls (n = 14): 236 +/- 69 micrograms/g creatinine. In six patients treated with intravenous thiamine, the elevated TPPE decreased to normal, from a mean (+/- SE) of 27.0 +/- 3.8% to 4.5 +/- 1.3% (p less than 0.001), indicating normal thiamine utilization capacity. Left ventricular ejection fraction increased in four of five of these patients studied by echocardiography. CONCLUSIONS: These preliminary findings suggest that long-term furosemide therapy may be associated with clinically significant thiamine deficiency due to urinary loss and contribute to impaired cardiac performance in patients with CHF. This deficit may be prevented or corrected by appropriate thiamine supplements.

Improved left ventricular function after thiamine supplementation in patients with congestive heart failure receiving long-term furosemide therapy.

PURPOSE: We have previously found thiamine (vitamin B1) deficiency in patients with congestive heart failure (CHF) who had received long-term furosemide therapy. In the present study, we assessed the effect of thiamine repletion on thiamine status, functional capacity, and left ventricular ejection fraction (LVEF) in patients with moderate to severe CHF who had received furosemide in doses of 80 mg/d or more for at least 3 months. PATIENTS AND METHODS: Thirty patients were randomized to 1 week of double-blind inpatient therapy with either i.v. thiamine 200 mg/d or placebo (n = 15 each). All previous drugs were continued. Following discharge, all 30 patients received oral thiamine 200 mg/d as outpatients for 6 weeks. Thiamine status was determined by the erythrocyte thiamine-pyrophosphate effect (TPPE). LVEF was determined by echocardiography. RESULTS: TPPE, diuresis, and LVEF were unchanged with i.v. placebo. After i.v. thiamine, TPPE decreased (11.7% +/- 6.5% to 5.4% +/- 3.2%; P < 0.01). LVEF increased (0.28 +/- 0.11 to 0.32 +/- 0.09; P < 0.05), as did diuresis (1,731 +/- 800 mL/d to 2,389 +/- 752 mL/d; P < 0.02), and sodium excretion (84 +/- 52 mEq/d to 116 +/- 83 mEq/d, P < 0.05). In the 27 patients completing the full 7-week intervention, LVEF rose by 22% (0.27 +/- 0.10 to 0.33 +/- 0.11, P < 0.01). CONCLUSIONS: Thiamine repletion can improve left ventricular function and biochemical evidence of thiamine deficiency in some patients with moderate-to-severe CHF who are receiving longterm furosemide therapy.

Subaortic stenosis: an unrecognized problem in transposition of the great arteries.

Right ventricular (subaortic) obstruction has only rarely been described in complete transposition of the great arteries. five patients with complete transposition of the great arteries in whom subaortic stenosis was angiocardiographically demonstrated were studied. All had a pressure gradient of 30 to 55 mm Hg across the aortic outflow tract. Two of the patients manifested mild tricuspid insufficiency, and another two had coarctation of the aorta. The etiologic, anatomic, hemodynamic and prognostic aspects of this unusual anomaly are discussed. An angiocardiographically demonstrated series of this anomaly has not been reported on before.

Two-dimensional echocardiography in discrete subaortic stenosis.

Thirty-seven patients with discrete subaortic stenosis (DSS) underwent 2-dimensional echocardiography (2-D echo) and cardiac catheterization. The peak systolic pressure gradients ranged from 0 to 150 mm Hg. Thirty-two patients had membranous DSS and 5 had fibromuscular DSS. Of 37 patients with DSS, 2-D echo diagnosed the presence and type in 35; in 2, a membrane was demonstrated by angiography. Of the 35 patients accurately diagnosed by 2-D echo, angiography corroborated the diagnosis in 33, but failed to show the membrane in 2. Subsequent cardiac surgery confirmed the accuracy of the echocardiographic diagnosis in these 2 patients. In all patients with membranous DSS, the anterior insertion of the membrane was demonstrated. In 9 of them the posterior insertion was demonstrated by tilt of the transducer but the anterior insertion disappeared. In 4 patients both insertions were demonstrated simultaneously and in 3 patients the membrane was demonstrated as a continuous line. In 4 of the 5 patients with fibromuscular DSS, both insertions of the lesion were demonstrated simultaneously. However, 2-D echo was unsuccessful in assessing the severity of obstruction. In only 1 patient did demonstration of the whole subaortic membrane as a continuous line below the aortic valve correlate with severe obstruction. Thus, the presence and type of DSS, but not the degree and severity, can be accurately and reliably diagnosed by means of 2-D echo.

Usefulness of heavy isometric exercise echocardiography for assessing left ventricular wall motion patterns late (> or = 6 months) after acute myocardial infarction.

The aim of this prospective study was to determine the effects of heavy isometric exercise on left ventricular (LV) wall motion patterns in patients who have had myocardial infarction, and to compare heavy isometric exercise with dynamic exercise for competence in eliciting LV wall motion abnormalities at equivalent rate-pressure products. Echocardiography was performed in 42 patients during supine bicycle ergometry and during heavy dynamometer stretching at 50% of maximal voluntary contraction. Systemic vascular resistance increased from 1,484 to 1,649 dynes s cm-5 (p < 0.05) during isometric exercise, and decreased significantly during dynamic exercise. Wall motion abnormalities or new asynergy were induced by isometric exercise in 120 segments, 107 of which (89%) showed significant stenosis of the perfusing coronary artery. Hypokinesia was the dominant pattern in the range of 76 to 90% narrowing; akinesia was dominant at 91 to 100% narrowing. Wall motion abnormalities were also documented in 13 segments (11%) assumed to be supplied by vessels with nonsignificant stenosis. Dyskinesia, seen in 7% of the segments, was equally distributed between both groups with significant stenosis. Sensitivity and positive predictive value in identifying specific coronary vessel disease was similar for both isometric and dynamic exercise. In conclusion, heavy isometric exercise in patients who have had myocardial infarction induces wall motion abnormalities of a severity proportional to the degree of coronary narrowing. This exercise method is similar to dynamic exercise for ability in identifying obstructions in a specific vessel. Furthermore, when compared at near-equal rate-pressure products, heavy isometric exercise is far superior in sensitivity to dynamic exercise.

Value of Holter monitoring in assessing cardiac arrhythmias in symptomatic patients.

Holter electrocardiographic monitoring in 55 symptomatic patients with syncope, palpitations or dizziness uncovered significant arrhythmias in 30 patients (55 percent). By providing an observation period of at least 24 hours including a period of sleep, the procedure aided detection and diagnosis in both symptomatic and asymptomatic patients of transient arrhythmias or conduction abnormalities not documented by routine electrocardiograms. Bradyarrhythmias accounted for the majority of arrhythmias recorded in 21 or 30 symptomatic patients (70 percent); 15 had sinus bradycardia (35 to 55 beats/min) alone and 6 also had long episodes of sinus arrest of up to 5 seconds. Two had sinus bradycardia with periods of atrioventricular block with Wenckebach phenomenon. Five patients had a tachycardia-bradycardia syndrome; three had other episodic arrhythmias and one had pacemaker failure. In 15 (60 percent) of the 25 patients without arrhythmias, monitoring did not document the cause of symptoms. Holter monitoring is of considerable value in assessing the efficacy and adequacy of drug treatment, especially in patients with known heart disease, and in detecting pacemaker malfunction. However, very long periods of monitoring may be needed to make a diagnosis in those with only sporadic symptoms.

Comparison of left ventricular function using isometric exercise Doppler echocardiography in competitive runners and weightlifters versus sedentary individuals.

It is unclear whether cardiovascular responses to heavy isometric exercise are changed by intensive training. We evaluated the effects of this type of exercise on left ventricular (LV) function in athletes engaged in static and dynamic sport, compared with sedentary persons, and looked for peculiarities in static athletes' responses that might reflect adaptive mechanisms to their specific activity. The study population comprised 45 men (age 24 +/- 5 years): 29 dynamic and 16 static athletes (runners and weightlifters, respectively). The control group consisted of 20 age and gender-matched healthy sedentary persons. All performed 50% of maximal voluntary contraction on a whole-body isometric exercise device for 2 minutes. Echocardiographic calculations were determined at rest and exercise. Upon exercise, stroke volume, cardiac output, end-diastolic volume, and ejection fraction increased significantly in athletes, while end-systolic volume and systemic vascular resistance decreased. In sedentary persons, stroke volume and resistance remained unchanged, cardiac output and LV volumes increased, and ejection fraction decreased from 67 +/- 5% to 60 +/- 5% (p <0.01 compared with rest; p <0.0001 compared with athletes). Whereas peak flow velocity decreased from 103 +/- 10 to 81 +/- 6 cm/s in sedentary persons, it increased from 112 +/- 9 to 126 +/- 8 cm/s in the static group and from 120 +/-3 to 126 +/- 9 cm/s in the dynamic athletes (p <0.0001 compared with the sedentary group). Mean acceleration decreased in the sedentary group, remained unchanged among the dynamic athletes, and increased among the static athletes. We conclude that cardiovascular responses to heavy isometric exercise are modified by intensive training. Athletes, taken as a group, react differently and adapt better than sedentary individuals. Moreover, among them, those involved in static sport show an improved cardiovascular adaptation to this type of exercise.

Comparison of coronary calcium in stable angina pectoris and in first acute myocardial infarction utilizing double helical computerized tomography.

Although coronary calcium is invariably associated with atherosclerosis, its role in the pathogenesis of acute and chronic coronary syndromes remains unclear. Utilizing double helical computerized tomography we evaluated the coronary calcium patterns in 149 patients: 47 with chronic stable angina (SAP) compared with 102 patients surviving a first acute myocardial infarction (AMI). Prevalence of coronary calcium was 81% among the AMI patients and 100% in the stable angina patients. The 547 calcific lesions identified in the AMI patients and the 1,242 lesions in the stable angina patients were categorized into 3 groups according to their extent: mild, intermediate, and extensive. The age-adjusted percentages of the highest level of calcification among AMI versus stable angina patients were: mild 18% vs 3%, intermediate 49% vs 18%, and extensive lesions 33% vs 79%, respectively (p < 0.01). In the AMI group, 73 culprit arteries were identified: 16 (22%) had no calcium detected, whereas 30 (41%) had mild lesions, 20 (27%) had intermediate forms, and only 7 (10%) had extensive lesions. The age-adjusted mean of the natural logarithm transformation of total calcium scores +1 was significantly lower in patients with AMI than in those with SAP (4.1 [95% confidence interval 3.7 to 4.4) vs 5.3 [95% confidence interval 4.8 to 5.8]). Thus, double helical computerized tomography demonstrates that extensive calcium characterizes the coronary arteries of patients with chronic stable angina, whereas a first AMI most often occurs in mildly calcified or noncalcified culprit arteries.

Randomized controlled trial of late in-hospital angiography and angioplasty versus conservative management after treatment with recombinant tissue-type plasminogen activator in acute myocardial infarction.

Although both the European Cooperative Study Group and the Thrombolysis in Myocardial Infarction IIB trial indicated that angiography and angioplasty as routine measures after thrombolytic treatment do not improve clinical outcome in patients with acute myocardial infarction, the potential benefit of angioplasty may have been negated by the fact that the procedure was performed too soon (less than 32 hours) after admission. A similar study was designed in which delayed invasive treatment was compared with conservative treatment in 201 patients with acute myocardial infarction given recombinant tissue-type plasminogen activator. The 97 patients randomized to the invasive group underwent routine coronary angiography and angioplasty 5 +/- 2 days after thrombolytic therapy, whereas the 104 patients randomized to the conservative group underwent angiography only for recurrent postinfarction angina or exercise-induced ischemia. Baseline characteristics of both groups were similar. In the invasive group, 92 patients underwent angiography, 49 angioplasty and 11 coronary artery bypass surgery. In the conservative group, 40 patients experienced early ischemia, 39 underwent angiography, 20 angioplasty and 4 coronary artery bypass surgery. Reinfarction rate and preservation of left ventricular function at discharge or 8 weeks after discharge did not differ in the 2 groups. Total mortality after a mean follow-up of 10 months was 8 of 97 in the invasive and 4 of 104 in the conservative groups (p = 0.15). However, if only patients who died after the timing of the scheduled protocol catheterization in the invasive arm were included, mortality was 5 of 94 and 0 of 100 in the invasive and conservative treatment groups, respectively (p = 0.02). (ABSTRACT TRUNCATED AT 250 WORDS)

Coronary calcium and anti-cardiolipin antibody are elevated in patients with typical chest pain.

The aim of this study was to examine whether detection of coronary calcium and the autoimmune response associated with atherosclerosis, either solely or in combination, are different in patients with typical and atypical chest pain. Coronary calcium as detected by spiral computerized tomography and levels of antibodies against cardiolipin (CL), oxidized low-density lipoprotein (ox-LDL), and beta2-glycoprotein-I (beta2-GPI) were studied in patients with typical chest pain (n = 52), atypical chest pain (n = 19), or without chest pain (n = 21). Patients with typical chest pain had higher mean levels of coronary calcium (expressed as natural transformation of total coronary calcium score) compared with patients with atypical chest pain and controls (5.04 vs 3.21 and 2.75, respectively; p < 0.001). The levels of anti-CL were (mean +/- SD of optical density multiplied by 1,000): 262 +/- 140, 170 +/- 82, and 230 +/- 115 for patients with typical chest pain, atypical chest pain, and controls, respectively (p = 0.016). No significant difference was found between groups regarding anti-ox-LDL and anti-beta2-GPI autoantibody levels. In the typical chest pain group, there was a higher prevalence of high total coronary calcium scores (p = 0.03) and high anti-CL levels (p = 0.01) than in the atypical chest pain group. Eighteen of 52 patients with typical chest pain (35%) had both high calcium scores and high antibody levels, whereas none of the 19 patients (0%) who had atypical chest pain had high levels of both (p = 0.003). A combination of both coronary calcium and anti-CL was associated with higher area under the receiver operator characteristic curves than for each separately. High coronary calcium scores or high anti-CL levels are found more often in typical than in atypical chest pain patients, but a combination of high levels of both can better differentiate typical from atypical chest pain patients.

Clinical impact of borderline and undiagnosed diabetes mellitus in patients with coronary artery disease.

The present study was aimed to evaluate the prevalence and prognostic significance of unrecognized and newly defined borderline diabetes (with fasting blood sugar 126 to 139 mg/dl) by the American Diabetes Association criteria in coronary patients over a 7.7-year follow-up. Both undiagnosed and newly diagnosed borderline diabetes were associated with an unfavorable metabolic profile. The mortality of the borderline diabetics tended to be higher than in their nondiabetic counterparts. but this tendency did not reach statistical significance. A significant excess in long-term mortality was observed among the undiagnosed diabetes group.