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Biomedical subjects

P Spirito

Publications and source records attributed to P Spirito.

69 records · Page 4Linked to original sources
PubMed1985

Prognostic significance and natural history of left ventricular thrombi in patients with acute anterior myocardial infarction: a two-dimensional echocardiographic study.

Fifty-eight patients with transmural anterior myocardial infarction were prospectively studied with serial two-dimensional echocardiography to determine the clinical implications and prognostic significance of detection of left ventricular thrombus during acute myocardial infarction, the incidence of systemic embolization, and the possible occurrence of spontaneous regression of left ventricular thrombi. Patients were not treated with anticoagulants or platelet inhibitors during the acute phase of infarction or during follow-up. Two-dimensional echocardiograms were obtained within 24 hr of myocardial infarction, every 24 hr until day 5, every 48 hr until day 15, and every month for a follow-up of 2 to 11 months (mean 7), in the surviving patients; a total of 774 echocardiograms were obtained. Left ventricular thrombi were identified in 24 (41%) of the 58 study patients, and developed within 48 hr of infarction in 11 of these patients. Ten (91%) of the 11 patients with early thrombus formation died during hospitalization or during follow-up, while only two (15%) of the 13 who developed a thrombus after 48 hr of infarction died (p less than .005). Incidence of Killip class III or IV, total lactic dehydrogenase values, and extent of wall motion abnormalities were significantly higher in patients who developed a thrombus within 48 hr of infarction than in patients without thrombus. On the other hand, in patients who developed a thrombus after 48 hr of infarction, these parameters were not significantly different from those in patients who did not develop a thrombus. Spontaneous regression of thrombi was documented in three (20%) of the 15 patients who survived the acute phase of myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Patterns of systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy: assessment by two-dimensional echocardiography.

A variety of patterns of systolic anterior motion (SAM) of the mitral valve were identified by realtime, 2-dimensional echocardiography in 62 patients with hypertrophic cardiomyopathy. In 36 patients (58%), both the anterior and posterior mitral leaflets appeared to participate importantly in SAM, although the anterior leaflet actually contacted or most closely approached the ventricular septum during systole because of its anterior anatomic position. In 19 patients (31%), SAM was produced selectively by the posterior mitral leaflet. In only 6 patients (10%) was the anterior leaflet alone responsible for SAM. In just 1 patient did the chordae tendineae appear to be primarily responsible for the SAM. In 51 patients (82%), only the distal portion of the anterior or posterior mitral leaflet (and possibly the attached proximal chordae tendineae) approached or contacted the septum in systole; in 10 patients both the body and tip regions of the anterior leaflet produced mitral-septal apposition. Hence, in obstructive hypertrophic cardiomyopathy, (1) the morphologic structures responsible for moderate to severe SAM are not identical in all patients, and a variety of patterns of SAM occur; (2) the posterior mitral leaflet plays an important role in SAM in almost 90% of patients, either by producing SAM alone (31%) or by moving anteriorly in concert with the anterior leaflet (58%); (3) SAM produced selectively by the anterior mitral leaflet is relatively uncommon; and (4) SAM is usually produced primarily by the distal portions of the mitral leaflets (with or without the attached chordae tendineae).

Adolescent↗
PubMed1984

Morphologic determinants of hemodynamic state after ventricular septal myotomy-myectomy in patients with obstructive hypertrophic cardiomyopathy: M mode and two-dimensional echocardiographic assessment.

To define the morphologic features of the left ventricle after ventricular septal myotomy-myectomy and to elucidate the structural changes associated with a postoperative reduction in the pressure gradient, 28 patients with obstructive hypertrophic cardiomyopathy were studied with M mode and qualitative and quantitative two-dimensional echocardiography. Nine patients with a marked reduction in the pressure gradient (no or small, less than or equal to 25 mm Hg, residual basal gradient) demonstrated a marked reduction in septal thickness after surgery (23 +/- 6 to 13 +/- 4 mm; p less than .01), a concomitant increase in septal to mitral valve distance (20 +/- 2 to 30 +/- 5 mm; p less than .005), and a loss or substantial decrease in the magnitude of systolic anterior motion of the mitral valve. Two-dimensional echocardiographic results demonstrated an increase of over 100% in the cross-sectional area of the left ventricular outflow tract at onset of systole (2.2 +/- 0.6 to 5.5 +/- 3 cm2; p less than .01). In six of the patients postoperative paradoxic septal motion appeared to contribute importantly to the increased size of the outflow tract during ventricular systole. In contrast, nine patients with little or no change in the pressure gradient (residual basal gradient greater than or equal to 40 mm Hg) demonstrated a less marked decrease in septal thickness and no significant change in septal to mitral valve distance or magnitude of mitral systolic anterior motion. Furthermore, the postoperative left ventricular outflow tract area was significantly smaller in patients with residual basal gradients (3.0 +/- 1 cm2) than that in patients with no residual gradient (5.5 +/- 3 cm2; p less than .05). Ten patients with only provocable subaortic gradients after operation showed postoperative left ventricular outflow tract dimensions intermediate between those in patients with either residual basal gradient or no residual gradient. On the basis of this echocardiographic assessment of septal myotomy-myectomy, we conclude that abolition or reduction of the subaortic gradient after operation in patients with obstructive hypertrophic cardiomyopathy is largely the consequence of surgical enlargement of the left ventricular outflow tract area.

Adolescent↗
PubMed1983

Relation of electrocardiographic abnormalities and patterns of left ventricular hypertrophy identified by 2-dimensional echocardiography in patients with hypertrophic cardiomyopathy.

Distribution of left ventricular (LV) hypertrophy was assessed by wide-angle, 2-dimensional (2-D) echocardiography in 153 patients with hypertrophic cardiomyopathy and compared with the scalar electrocardiogram in the same patients. The most common electrocardiographic alterations were S-T segment changes and T-wave inversion (61%), LV hypertrophy (47%), abnormal Q waves (25%), and left atrial enlargement (24%). LV hypertrophy on the electrocardiogram was significantly more common in patients with the most extensive distribution of LV hypertrophy on 2-D echocardiogram involving substantial portions of both the ventricular septum and LV free wall (type III; 51 of 69, 74%) than in those with more limited distribution of LV hypertrophy (21 of 84, 25%; p less than 0.001). Most patients with hypertrophic cardiomyopathy and normal electrocardiograms (13 of 23) had localized (type I) hypertrophy, but only 4 had the extensive type III pattern of hypertrophy. Abnormal Q waves were significantly more common in those patients without hypertrophy of the anterior, basal septum (type IV; 15 of 27, 56%) than in those with basal septal hypertrophy (23 of 126, 18%; p less than 0.001); abnormal Q waves were uncommon in extensive type III distribution of hypertrophy (13 of 69, 19%). Thus, although no single electrocardiographic abnormality is characteristic of hypertrophic cardiomyopathy, 2-D echocardiography clarifies the significance of certain electrocardiographic patterns: (1) LV hypertrophy on the electrocardiogram, although present in only about half of the study group, was a relatively sensitive (74%) marker for extensive (type III) LV hypertrophy; (2) abnormal Q waves cannot be explained by ventricular septal hypertrophy alone; and (3) a normal electrocardiogram was most commonly a manifestation of localized LV hypertrophy.

Adolescent↗
PubMed1983

Prevalence and significance of an abnormal S-T segment response to exercise in a young athletic population.

Treadmill stress electrocardiography is employed widely to detect underlying cardiovascular disease in asymptomatic persons. To determine the frequency and significance of an abnormal S-T segment response to exercise in young athletes with increased left ventricular (LV) mass induced by physical conditioning, 75 male isometrically trained athletes without evidence of heart disease (mean age 21 years) and 48 nonathletic young normal subjects were studied by M-mode echocardiography and exercise electrocardiography. Ventricular septal and posterior free wall thicknesses and calculated LV mass were significantly greater in athletes than in control subjects. An abnormal S-T segment response to exercise was present in 7 (9%) of the 75 athletes, all of whom had a LV mass greater than 275 g and in 5 the LV mass was above the 95th percentile of that of the control subjects. An abnormal treadmill exercise test result also was present in 3 (6%) of 48 control subjects. Seven of the 10 subjects with abnormal exercise test results had radionuclide angiograms at rest and with exercise, each of which was normal. It is concluded, therefore, that (1) abnormal exercise test results occur commonly in both athletes and non-athletes; (2) almost 10% of isometrically trained athletes have "false-positive" exercise electrocardiograms, suggesting that this test has major limitations in screening for underlying cardiovascular disease in athletes; and (3) in athletes, a relation was present between "physiologically" increased LV mass and false-positive exercise test results.

Adolescent↗
PubMed1983

Significance of left ventricular outflow tract cross-sectional area in hypertrophic cardiomyopathy: a two-dimensional echocardiographic assessment.

The morphologic determinants of subaortic obstruction in patients with hypertrophic cardiomyopathy are not completely understood. To define the relation between left ventricular outflow tract orifice size and presence or absence of subaortic obstruction, we studied 65 patients with hypertrophic cardiomyopathy and 16 normal controls by quantitative two-dimensional echocardiography. Left ventricular outflow tract area was measured at the onset of systole in the short-axis view in the stop-frame mode. Left ventricular outflow tract area was significantly smaller in patients with hypertrophic cardiomyopathy and subaortic obstruction (2.6 +/- 0.7 cm2) than in patients without obstruction (5.9 +/- 1.6 cm2, p less than 0.001). Twenty of 21 patients with obstruction had a left ventricular outflow tract area smaller than 4.0 cm2, whereas 28 of 30 patients without obstruction had a left ventricular outflow tract area of 4.0 cm2 or greater. The outflow tract area in patients with provocable obstruction (4.6 +/- 1.6 cm2) was intermediate between the areas of patients with and without obstruction. Left ventricular outflow tract area was significantly smaller in patients with hypertrophic cardiomyopathy (4.6 +/- 2.0 cm2) than in normal subjects (10.4 +/- 1.2 cm2, p less than 0.001). We conclude that the cross-sectional outflow tract area is closely related to the presence or absence of subaortic obstruction in patients with hypertrophic cardiomyopathy. Hence, the size of the outflow tract at the level of the mitral valve appears to be of major pathophysiologic significance in producing obstruction in these patients.

Adolescent↗
PubMed1983

Systolic anterior motion of the posterior mitral leaflet: a previously unrecognized cause of dynamic subaortic obstruction in patients with hypertrophic cardiomyopathy.

Dynamic obstruction to left ventricular outflow in patients with hypertrophic cardiomyopathy usually occurs when the anterior mitral leaflet moves forward in systole and approaches or contacts the ventricular septum. However, we have recently identified, by M mode and two-dimensional echocardiography, 21 patients with hypertrophic cardiomyopathy who had a unique pattern of mitral valve motion characterized by abnormal mitral valve coaptation and systolic anterior motion of the posterior mitral leaflet. This abnormality of mitral valve motion was most reliably identified with two-dimensional echocardiography in views of the left ventricle obtained from the apex. At end-diastole the anterior and posterior mitral leaflets did not appear to coapt at their distal free margins. Rather, at mitral valve closure, the anterior mitral leaflet contacted the basal portion of posterior mitral leaflet. Subsequently, during systole the "residual" distal portion of posterior mitral leaflet approached or contacted the ventricular septum. Morphologic observations in nine other patients with hypertrophic cardiomyopathy suggested that systolic anterior motion of the posterior mitral leaflet is due to elongation of the middle scallop of the posterior leaflet, which probably comes into apposition with the ventricular septum during systole by passing through the space created by the normal pattern of chordal attachments onto the anterior mitral leaflet. Of the 16 patients who underwent cardiac catheterization, nine had basal subaortic gradients of 20 to 85 mm Hg, which were apparently due to moderate or marked systolic anterior motion of the posterior mitral leaflet. Ventricular septal myotomy-myectomies were performed in two patients and resulted in markedly diminished systolic anterior motion of the posterior mitral leaflet in each and abolition of subaortic gradient in the one patient who underwent postoperative cardiac catheterization. Hence, in patients with hypertrophic cardiomyopathy, systolic anterior motion of the posterior mitral leaflet (1) is not uncommon (identifiable in about 10% of a consecutively studied series of patients), (2) constitutes a previously undescribed mechanism for dynamic subaortic obstruction, and (3) is due to a malformation of the posterior mitral leaflet.

Adolescent↗
PubMedDate not supplied

A mutant tropomyosin that causes hypertrophic cardiomyopathy is expressed in vivo and associated with an increased calcium sensitivity.

Mutant contractile protein genes that cause familial hypertrophic cardiomyopathy (FHC) are presumed to encode mutant proteins that interfere with contractile function. However, it has generally not been possible to show mutant protein expression and incorporation into the sarcomere in vivo. This study aimed to assess whether a mutant alpha-fast tropomyosin (TM) responsible for FHC is actually expressed and determines abnormal contractile function. Since alpha-fast TM is expressed in heart and skeletal muscle, samples from vastus lateralis muscles were studied from two FHC patients carrying an Asp175Asn alpha-fast TM mutation and two healthy control subjects. TM isoforms from whole biopsy samples and single fibers were identified by gel electrophoresis and Western blot analysis. An additional faster-migrating TM band was observed in both FHC patients. The aberrant TM was identified as the Asp175Asn alpha-fast TM by comigration with purified recombinant human Asp175Asn alpha-fast TM. Densitometric quantification of mutant and wild-type alpha-fast TMs suggested equal expression of the two proteins. Contractile parameters of single skinned muscle fibers from FHC patients and healthy control subjects were compared. Calcium sensitivity was significantly increased in muscle fibers containing Asp175Asn alpha-fast Tm compared with fibers lacking the mutant TM. No discernible difference was found regarding cooperativity, maximum force, and maximum shortening velocity. This is the first demonstration that the mutant TM that causes FHC is indeed expressed and almost certainly incorporated into muscle in vivo and does result in altered contractile function; this confirms a dominant-negative, rather than null allele, action. Since the mutant TM was associated with increased calcium sensitivity, this mutation might be associated with an enhancement and not a depression of cardiac contractile performance. If so, this contrasts with the hypothesis that FHC mutations induce contractile impairment followed by compensatory hypertrophy.

Adult↗
PubMedDate not supplied

Higher pregnancy rates following treatment of cervical factor with intrauterine insemination without superovulation versus intercourse: the importance of a well-timed postcoital test for infertility.

A randomized study comparing the efficacy of timed intrauterine insemination (IUI) without hyperstimulation to sexual intercourse was performed in women with cervical factor infertility. Among the strict requirements for inclusion in the study were a normal semen analysis in the male partner, as well as the failure to demonstrate any sperm with progressive forward motion in a postcoital test performed 8-12 h after intercourse at the time of a mature follicle. All other infertility factors were negative. The data demonstrated a statistically significant fecundity rate at 1 month when IUI was compared to intercourse (21.2 vs. 3.9%). These data suggest that carefully timed IUI in nonhyperstimulated cycles is an effective treatment for cervical factor infertility.

Bromocriptine↗
PubMedDate not supplied

[Ventricular arrhythmia in a group of patients with hypertrophic cardiomyopathy].

A possible connection between M-mode echocardiographs and the incidence of ventricular arrhythmias was investigated in a group of patients with hypertrophic cardiomyopathy. No single echocardiographic parameter could identify the patients with serious ventricular arrhythmias. Multivaried discriminatory analysis revealed the extent of the septal excursion, the telediastolic thickness of the interventricular septum, the E-F incline and the dimension of the left atrium as the most significant echocardiographic features identifying patients with serious ventricular arrhythmias.

Adult↗
PubMedDate not supplied

[Evaluation of the cardiovascular effects of the beta-blockader atenolol].

The beta-blocking action of 100 mg per diem Atenol was evaluated in 8 patients with conditions requiring treatment with a beta-blocking drugs (ischaemic cardiopathy, arterial hypertension, hypertrophic myocardiopathy). Ergometer bicycle exertion tests were used to evaluate the extent of Atenol's beta-blocking action (in basal condition, 3 and 24 hours after administration of the drug) as well as Holter type dynamic ECG recordings (basal and under treatment). The drug significantly reduced cardiac frequency and arterial pressure both at rest and under exertion. It also significantly reduced average hourly and daily cardiac frequency as shown by dynamic ECG. No side effects of the drug were observed.

Adult↗