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Biomedical subjects

H Boudoulas

Publications and source records attributed to H Boudoulas.

At least 91 records · Page 5Linked to original sources
PubMed1989

Biphasic pattern of hypersensitivity following acute propranolol withdrawal in normal subjects.

The effect of abrupt propranolol withdrawal on exercise-induced changes in heart rate and blood pressure was studied in six normal volunteers. Response to exercise was measured on two occassions during propranolol treatment and 1, 2, 3, 4, 5 and 7 days after the last dose of propranolol. Exercise-induced changes in heart rate were significantly lower than control during propranolol treatment (p less than 0.005). Following propranolol cessation, all subjects showed a biphasic pattern of hypersensitivity. Heart rate response was significantly greater than control 2, 3 and 7 days after the last propranolol dose (p less than 0.05) and not significantly different from control 1, 4 and 5 days after the last dose of propranolol. Exercise-induced changes in pulse pressure showed a biphasic pattern similar to the changes in heart rate.

Adult↗
PubMed1989

Functional abnormalities in isolated left bundle branch block. The effect of interventricular asynchrony.

Eighteen patients with isolated left bundle branch block (LBBB) were compared with 10 normal control subjects. Apexcardiograms, phonocardiograms, electrocardiograms, two-dimensional and dual M-mode echocardiograms, and radionuclide ventriculograms (RNV) were performed. There were no differences in the timing of right ventricular events between LBBB and normal subjects; however, striking delays in left ventricular systolic and diastolic events were apparent in the LBBB group. The delay was associated with shortening of left ventricular diastole and resultant increase in the ratio of right to left ventricular diastolic time in LBBB (1.2 +/- 0.08) compared with normal (1.0 +/- 0.06), p less than 0.0001. First heart sound (S1) amplitude, expressed as the ratio S1/S2, was decreased in LBBB compared with normal (0.67 +/- 0.2 compared with 1.34 +/- 0.25, p less than 0.01), in part due to wide separation of the valvular contributors to S1. The abnormal interventricular septal motion in LBBB corresponded to periods of asynchrony in contraction, ejection, end systole, and end diastole between right and left ventricles. Radionuclide ventriculograms revealed decreased regional ejection fraction of the septum in LBBB (40 +/- 16%) compared with 67 +/- 7% in normal subjects (p less than 0.001), while the apical and lateral regional ejection fractions were similar in the two groups. This loss of septal contribution resulted in a reduction in global ejection fraction in LBBB compared to normals (54 +/- 7% compared with 62 +/- 5%, p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Syncope in dental practice.

This article will provide an overview of the pathophysiologic mechanism and management of syncope. It will discuss the classifications and varieties of syncope, as well as syncope caused by dental practices. Finally, the authors will suggest management options for syncope.

Dental Care↗
PubMed1989

Segmental analysis of the ascending aorta: definition of normality and classification of aortic dilatation.

To better define and classify ascending aortic abnormalities, we adapted the left ventricular dynamic segmental analysis concept to the ascending aorta. Ascending aortic diameters were measured from contrast aortography in 18 normal subjects at the aortic valve (level 1), and 2, 4, and 6 cm above the aortic valve (levels 2, 3, and 4). Diameters greater than two standard deviations (SD) above the mean normal values at any levels were considered abnormal. Aortograms of 102 consecutive patients with abnormal aorta were analyzed. Three patterns of aortic dilatation were identified: I (n = 55), the largest aortic diameter was at level 2 (normal pattern); II (n = 39), the aortic diameters increased from levels 1 to 4; III (n = 8), all aortic diameters were greater than 2 SD above the mean normal values and increased from levels 1 to 4. Segmental analysis of the aorta provides an objective comparative basis for definition and classification of aortic dilatation and aneurysm.

Adult↗
PubMed1988

Mitral valve prolapse syndrome. Evidence of hyperadrenergic state.

Although mitral valve prolapse (MVP) is a common valvular abnormality, its diagnostic classification has not been well defined. MVP is considered to be an anatomic entity with specific pathologic tissue characteristics and pathophysiologic consequences. The term "MVP syndrome" (MVPS) is used to refer to symptoms due to neuroendocrine or autonomic dysfunction that occur in patients with MVP and that cannot be explained on the basis of valvular abnormality alone. Several studies have shown that patients with MVPS have high urinary epinephrine and norepinephrine excretion, high plasma catecholamine concentrations, abnormal catecholamine response to volume expansion, and hyperresponse to adrenergic stimulation. In patients with MVPS and ventricular arrhythmias, the frequency of premature ventricular contractions parallels the urinary and plasma catecholamine values. The clinical presentation of MVPS may be related in part to high adrenergic tone and/or hyperresponse to adrenergic stimulation. Therefore, certain patients with MVPS and high adrenergic tone may benefit from beta blockade.

Adrenergic beta-Antagonists↗
PubMed1988

Mitral stenosis: mitral dome excursion at M1 and the mitral opening snap--the concept of reciprocal heart sounds.

The dynamics of the delayed accentuated mitral component (M1) of the first heart sound and the MOS were studied in 11 patients with mitral stenosis of varying severity. Echophonocardiographic (M-mode and 2D) studies were performed with analysis of LA dimensions, dynamics, and mitral valve excursion at the time of M1 and MOS. LA area and length, mitral annular diameter, and mitral dome area (from anulus plane to fused valve tip) and length were measured at M1 and MOS. Significant dynamic increases in mitral dome area and length occurred from M1 to MOS, with less striking but consistent increases in LA area, LA length, and mitral annular diameter. Conversely, mitral dome area and length decreased significantly from MOS to M1, with less striking but consistent decreases in LA area, LA length, and mitral annular diameter. Frame-by-frame video tape analysis showed that dome movement was separate from anulus motion. Mitral dome descent into the left ventricle terminated at MOS and reversal of dome motion terminated at M1. The conformational and dimensional changes that terminated abruptly at MOS reversed and terminated abruptly in a reciprocal manner at the time of the delayed, accentuated M1. When considered in light of known hemodynamic, pressure pulse, and imaging correlates in mitral stenosis, these observations strengthen the hypothesis that the mechanisms involved in the production of M1 and MOS in mitral stenosis are paired or reciprocal in nature, and the delayed, accentuated M1 and the MOS of mitral stenosis are reciprocal cardiovascular sounds.

Adult↗
PubMed1988

Postural exercise abnormalities in symptomatic patients with mitral valve prolapse.

The hemodynamics of the supine and upright exercise response in 16 symptomatic women with mitral valve prolapse (Group I) was compared with that in 8 asymptomatic normal control women (Group II). All subjects had supine and upright echocardiography and phonocardiography at rest and none demonstrated mitral regurgitation. All participants then underwent same day graded bicycle exercise, with simultaneous radionuclide angiography in both the upright and the supine posture. Catecholamines were measured, and a variety of volumetric and hemodynamic data were obtained. Group I (patients with mitral valve prolapse) demonstrated a reduced exercise tolerance, especially during upright exercise, as measured by both total exercise duration and maximal work load achieved. Mean total catecholamine measurements were similar between the two study groups at comparable mean heart rate, mean blood pressure and mean rate-pressure (double) product. No difference was observed in the ratio of right to left ventricular stroke counts at rest or during exercise regardless of posture, suggesting that exercise-induced mitral regurgitation did not occur. A difference was noted, however, in left ventricular end-diastolic volume index. At rest, Group I patients exhibited a 42% decrease in this index when sitting upright, and this difference from supine values persisted at submaximal (300 kpm/min) and peak work loads (34 and 29% difference, respectively). This contrasted with the control subjects whose upright end-diastolic volumes at rest, at 300 kpm/min and at peak exercise were reduced 21, 10 and 3%, respectively, compared with supine values. Cardiac index measurements reflected the reduced left ventricular end-diastolic volume observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Floppy mitral valve chordae tendineae: histopathologic alterations.

Pathologic studies of floppy or myxomatous mitral valves have focused primarily on changes in the valve cusps, with little attention given to the chordae tendineae. In a systematic study of the histopathology of floppy mitral valve chordae tendineae, 128 nonruptured chordae from 8 severely regurgitant floppy mitral valves were compared to 152 chordae from 10 normal control mitral valves and to 152 chordae from 8 control mitral valves with severe regurgitation due to ischemic heart disease. Collagen alterations were observed in 2% of normal mitral valve chordae and 3% of control regurgitant mitral valve chordae compared to 38% of floppy mitral valve chordae. Moderate or severe acid mucopolysaccharide accumulation was observed in 2% of normal mitral valve chordae and 3% of control regurgitant mitral valve chordae compared to 39% of floppy mitral valve chordae. Nonuniform histopathologic alterations, rare in normal and control regurgitant mitral valve chordae tendineae, were frequent in floppy mitral valve chordae tendineae (p less than 0.001). Histopathologic alterations provide the basis for abnormal physical properties previously demonstrated in floppy mitral valve chordae tendineae and may predispose to chordal elongation and rupture.

Aged↗
PubMed1988

Mitral valve prolapse syndrome: neuro-endocrinological aspects.

Based on analysis of 399 symptomatic patients with mitral valve prolapse (MVP) and the reported experience of others, we developed a clinical classification in order to improve nosology, provide better identification and promote insight into the mechanism of symptoms in patients with MVP. The heading of anatomic MVP designates those in whom symptoms or complications were primarily or directly related to valvular dysfunction and the heading of MVP syndrome designates those patients in whom symptoms cannot be explained on the basis of valvular dysfunction alone. Patients with MVP syndrome present with a symptom complex which results from various forms of neuroendocrine or autonomic dysfunction; the most common symptoms include chest pain, palpitations, cardiac arrhythmias, orthostatic phenomena, syncope, presyncope, fatigue, exercise intolerance, dyspnea and neuropsychiatric symptoms (Table 1). Mechanisms underlying the condition have been shown to include increased adrenergic activity, disturbances of catecholamine regulation, hyperresponsiveness to adrenergic stimulation, anomalous beta-adrenergic receptors, dysfunction of the parasympathetic portion of the autonomic nervous system, disturbances in renin-aldosterone regulation, decreased intravascular volume, diminished left ventricular diastolic volume in the upright position as well as abnormal secretion of atrial natriuretic factor (Table 2). In MVP syndrome, alterations of the heart, kidney, the adrenals and the autonomic nervous system coexist and interact, creating a complex "neuro-endocrine cardiovascular process" which may account for many of the symptoms otherwise unexplained on the basis of the valvular abnormality alone.

Arousal↗
PubMed1988

Aortic distensibility in post-stenotic aortic dilatation: the effect of co-existing coronary artery disease.

Aortic distensibility is decreased in patients with coronary artery disease (CAD) and the angiographically normal aorta. To determine if the same is true in patients with aortic stenosis and post-stenotic dilatation, two groups were studied. Group A consisted of 15 patients with post-stenotic aortic dilatation and normal coronary arteries, and group B, 14 patients with post-stenotic aortic dilatation and CAD. The patients were compared to 18 normal subjects. The area of the first 6 cm of the aorta above the valve obtained by aortography was planimetered and the mean diameters were calculated. Distensibility was calculated using the formula: (formula; see text) Distensibility was greater in group A (2.5 +- .4 cm2.dynes-1) compared to group B (1.0 +- 8 cm2.dynes-1, p less than 0.001). Distensibility in normal subjects reported recently from this laboratory (3.4 +- .4 cm2.dynes-1) was greater compared to both groups A and B (p less than 0.001). Thus, distensibility was decreased in patients with post-stenotic aortic dilatation. The further decrease in distensibility in patients with co-existing coronary artery disease may be partially related to abnormal nutrition of the arterial wall since the vasa vasorum of the ascending aorta are derived from the coronary arteries.

Adult↗
PubMed1987

Aortic distensibility abnormalities in coronary artery disease.

Vasodilatory capacity of nonstenotic arteries in experimental animals with atherosclerosis is decreased. It was postulated that aortic distensibility may be abnormal in patients with coronary artery disease (CAD). Aortic distensibility was determined in 24 normotensive patients with CAD and an angiographically normal aorta and values were compared with those in 18 age-matched normal subjects. Aortic diameters were measured at 3 levels--2, 4 and 6 cm above the aortic valve--by angiographic techniques. The area of the first 6 cm of the aorta above the aortic valve was planimetered and mean aortic diameters were calculated. Distensibility was calculated using the formula: [2 X (changes of the aortic diameter)/(diastolic aortic diameter) X (changes of the aortic pressure)]. CAD patients had similar aortic pressures but markedly lower distensibility than normal subjects: 0.7 +/- 0.2 vs 1.7 +/- 0.3 (p less than 0.02); 1.5 +/- 0.3 vs 4.0 +/- 0.6 (p less than 0.02); and 1.2 +/- 0.2 vs 5.3 +/- 0.6 (p less than 0.001) at 2, 4 and 6 cm above the aortic valve, respectively. Distensibility was also calculated from the mean aortic diameters and was greater in normal subjects than in CAD patients (3.4 +/- 0.4 vs 1.6 +/- 0.1, p less than 0.001). Decreased aortic distensibility in CAD may be related to the common atherosclerotic process or to reduced ascending aorta vasa vasorum flow from coronary arteries.

Adult↗
PubMed1987

The equilibrium position of the mitral valve: an accurate model of mitral valve motion in humans.

A "semiopen" diastolic equilibrium position of the mitral valve that is assumed in the absence of transmitral flow has been demonstrated in instrumented dogs. It has been suggested that the papillary muscles and chordae tendineae play an integral role in returning the valve to this position after initial diastolic opening. To determine whether such a model of mitral valve motion is valid in noninstrumented humans without underlying valvular disease, M-mode and Doppler ultrasound studies were performed in 6 subjects who underwent prolonged periods of ventricular diastole and atrial inactivity. After maximal opening, the mitral valve assumed a stable open position in which mean separation of the anterior and posterior mitral leaflets was 52% of maximal separation. This position was maintained for a mean duration of 585 ms, during which time transmitral flow fell to 0 m/s. Peak mitral valve opening preceded the early transmitral flow peak by an average of 42 ms, suggesting an active closure of the mitral valve as flow continued to accelerate. It is concluded that a semiopen equilibrium position of the mitral valve is assumed during prolonged diastolic periods in the absence of transmitral flow and is an accurate model describing diastolic mitral valve motion in noninstrumented humans. The chordae tendineae and papillary muscles may actively participate in the genesis and maintenance of the equilibrium position.

Adult↗
PubMed1987

Reversed-phase liquid chromatography method for measurement of procainamide and three metabolites in serum and urine: percent of dose excreted as deethyl metabolites.

We report a reversed-phase high-performance liquid chromatography method for the determination of procainamide (PA) and three of its metabolites, n-acetylprocainamide (NAPA), deethylprocainamide (DEPA), and deethyl-n-acetylprocainamide (DENAPA), in serum and urine. (p-Amino)-n-(2-dipropylaminoethyl)-benzamide was the internal standard. A phenyl column (1.0-mL/min flow rate) and a mobile phase consisting of 0.075 M acetate buffer (pH 4.3):acetonitrile (20:3) resulted in a total chromatography time of 21.6 min. The optimum detector wavelength was 270 nm. Maximum linear concentrations were 37.8, 34.2, 20.0, and 16.3 mg/L for DEPA, DENAPA, PA, and NAPA, respectively. Minimum detectable concentrations were 0.05 mg/L or less for all four compounds. One-tenth milliliter of sample was extracted into methylene chloride:2-propyl alcohol (9:1). Extraction efficiencies were independent of concentration or biological fluid for each compound. Standard curves were linear and best-fit by dividing the curve into two portions and/or using weighted linear regression. Within-day and day-to-day precison were excellent. No interfering substances were observed in the serum or urine of normal subjects with the exception of caffeine, which was resolved by alteration of the mobile phase. Advantages of this method include a small sample volume, low minimum detectable concentrations, and an order of elution which enhances the detectability of the deethyl metabolites. Urinary excretion of DEPA and DENAPA accounted for an average of only 0.58 and 0.53%, respectively, of PA doses administered intravenously to six normal volunteers.

Acecainide↗
PubMed1987

Diastolic time in congestive heart failure.

Diastolic perfusion time is an important determinant of coronary blood flow and subendocardial perfusion. It has been proposed that subendocardial ischemia may exacerbate and perpetuate left ventricular dysfunction in congestive heart failure. Diastolic perfusion time in relation to heart rate was analyzed in 29 digitalized (group 1) and 12 nondigitalized patients (group 2) with heart failure and in 58 normal control subjects. In group 1 there was a strong negative exponential correlation (r = -0.85) and in group 2 a strong negative logarithmic correlation (r = -0.95) between heart rate and diastolic time; both regressions differed significantly from normal control. There was a 9% increase of diastolic time at a heart rate of 60 bpm in group 1 and a 7% increase in group 2 (both p less than 0.05) compared with normal subjects. The curves intersected the regression line of normal subjects at a heart rate of 98 bpm in group 1 and 93 bpm in group 2. At 120 bpm there was a 10% decrease in diastolic time for both groups with heart failure (both p less than 0.05). Changes in diastolic perfusion time relative to heart rate are more pronounced in congestive heart failure such that at faster heart rates this relationship may further impede subendocardial blood flow.

Adult↗
PubMed1987

Cardiovascular disease of connective tissue origin.

Inherited abnormalities of connective tissue elements often cause changes in the structure and function of the cardiovascular system. Well-known heritable disorders of connective tissue in which cardiovascular abnormalities are prominent include the Marfan syndrome and the Ehlers-Danlos syndrome. Connective tissue abnormalities also occur without the associated features of a recognized syndrome. These include isolated valvular prolapse and anuloaortic ectasia. In this review, the cardiovascular features of connective tissue abnormalities--both the recognized syndromes and the isolated abnormalities--are described, important concepts in the diagnosis and treatment of these disorders are reviewed, and the classification of inherited connective tissue abnormalities of the cardiovascular system is discussed.

Cardiovascular Diseases↗