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Biomedical subjects

J F Goodwin

Publications and source records attributed to J F Goodwin.

At least 37 records · Page 2Linked to original sources
PubMed1986

Muscle dynamics in hypertrophic cardiomyopathy.

Previous reports have demonstrated that patients with hypertrophic cardiomyopathy (HCM) have prolonged isovolumic relaxation period (IRP) reflecting reduced rate of fall of left ventricular pressure. Eighty four patients with proven hypertrophic cardiomyopathy and 31 normal subjects were studied by simultaneous recordings of echocardiogram, apexcardiogram, phonocardiogram and ECG. In normal subjects the IRP value was 61 +/- 11 ms (mean +/- s.d.). In the 84 patients there was enormous variability of the IRP value from 0 to 160 ms reflecting abnormal and incoordinate (but not necessarily impaired) relaxation and it was possible to identify three subgroups among the patients: 60 patients in sinus rhythm who had prolonged IRP and significantly above the normal values, 9 patients in atrial fibrillation in whom the IRP was within the normal range and 15 patients with IRP values between 0-45 ms, with the mean (26 ms) below the normal range (mean +/- 2 s.d.). This group of patients with short IRP also had signs of outflow tract systolic pressure gradient, with partial mid-systolic closure of the aortic valve, systolic anterior motion of the anterior mitral valve leaflet and paradoxical splitting of the second heart sound. It is suggested that the short IRP is due to extremely delayed aortic valve closure and careful scrutiny of this subset with haemodynamic evaluation has shown that this non-invasive interval (A2-Mo) may not always be a valid measure of left ventricular relaxation.

Adolescent↗
PubMed1985

Mechanisms in cardiomyopathies.

The three main clinical types of cardiomyopathy are: hypertrophic cardiomyopathy; dilated cardiomyopathy; and restrictive cardiomyopathy. In each case the basic cellular mechanisms still remain to be defined.

Adrenergic beta-Antagonists↗
PubMed1985

Relation of left ventricular function and prognosis in hypertrophic cardiomyopathy: an angiographic study.

Left ventricular cineangiograms performed at the time of diagnosis in 88 patients with hypertrophic cardiomyopathy were digitized to evaluate the relation of left ventricular function and prognosis in hypertrophic cardiomyopathy. Eleven patients died suddenly after a mean follow-up period of 7.5 +/- 7 years, 10 patients died of congestive heart failure or after cardiac surgery and 67 were alive after a mean follow-up period of 8.6 +/- 4 years. Measurements of left ventricular volume, ejection fraction, peak rate of ejection and filling and time to peak rate of ejection and filling were derived from curves of ventricular volume and its rate of change during the cardiac cycle. Patients who died suddenly had a lower peak rate of ventricular ejection (stroke volume-normalized peak ejection rate 5.41 +/- 0.69 versus 6.24 +/- 1.33 s-1; p = 0.006) and lower peak rate of ventricular filling (end-diastolic volume-normalized peak filling rate 4.02 +/- 0.94 versus 4.88 +/- 1.53 s-1; p = 0.02) and stroke volume-normalized peak filling rate (4.75 +/- 1.08 versus 5.82 +/- 1.70 s-1; p = 0.01) compared with survivors. Stepwise regression analysis revealed that sudden death was best predicted by the combination of increased end-diastolic volume, small end-systolic volume and low peak filling rate (predictive accuracy 32%, false negative 18% and false positive 28%). The addition of clinical features and hemodynamic measurements to the analysis improved predictive accuracy to 43% (false negative 18% and false positive 18%). Ambulatory electrocardiographic monitoring performed in 57 of the 88 patients 1 month to 17 years (median 8 years) after diagnosis revealed ventricular tachycardia in 14 (25%). Of these, 10 who survived had hyperkinetic systolic function at diagnosis, whereas the 4 who died suddenly had impaired systolic function (end-diastolic volume-normalized peak ejection rate 5.93 +/- 1.2 versus 4.01 +/- 1.2 s-1, respectively; p = 0.04). In hypertrophic cardiomyopathy, ventricular tachycardia is a sensitive but nonspecific marker of adults who are at risk of sudden death. Impaired systolic function may be an important determinant of which patients with ventricular tachycardia die suddenly. This study shows that indexes of ventricular function contribute to the identification of patients at particular risk of sudden death. However, the predictive power of the clinical features and hemodynamic and angiographic measurements that could be assessed was poor.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1985

Improved survival with amiodarone in patients with hypertrophic cardiomyopathy and ventricular tachycardia.

The effect of amiodarone on survival was assessed in patients with hypertrophic cardiomyopathy and ventricular tachycardia in a drug trial with historical controls. During 1976 and 1977, 24 hour (seven) or 48 hour (79) electrocardiographic monitoring was performed in 86 consecutive patients; 24 had ventricular tachycardia and received conventional antiarrhythmic agents. Nineteen clinical, echocardiographic, and haemodynamic features were assessed. Seven patients died suddenly during follow up of three years; of these, five had continued to have ventricular tachycardia and two had no documented ventricular tachycardia. During 1978 and 1979, ventricular tachycardia was detected during 48 hour electrocardiographic monitoring in 21 of the next 82 consecutive patients with hypertrophic cardiomyopathy. They received amiodarone (150-400 mg/day, median 300); ventricular tachycardia was suppressed in all during repeat 48 hour electrocardiographic examination. Two patients died suddenly during a three year follow up, but neither belonged to the amiodarone treated group with ventricular tachycardia. The clinical and haemodynamic variables were similar in patients taking amiodarone and conventional agents. The fact that control of ventricular arrhythmia with amiodarone is significantly associated with improved survival suggests that amiodarone may prevent sudden death in patients with hypertrophic cardiomyopathy and ventricular tachycardia.

Amiodarone↗
PubMed1984

Amiodarone for long-term management of patients with hypertrophic cardiomyopathy.

Fifty-three patients with hypertrophic cardiomyopathy who had serious arrhythmias (45 patients), refractory chest pain (5 patients) or a high risk of sudden death (3 patients) received amiodarone for 6 to 96 months (median 18) after completion of a loading and an initial maintenance period. The dose of amiodarone was altered by 50 to 200 mg/day at 3- to 6-month intervals, guided by electrocardiographic monitoring, plasma drug level measurements and side-effect questionnaires. Ventricular tachycardia was suppressed in 24 patients (92%) with doses of 100 to 400 mg/day (median 300); none died suddenly during a mean follow-up of 27 months. Although symptomatic episodes of frequent or prolonged supraventricular tachycardia or paroxysmal atrial fibrillation/flutter were abolished in 8 of 9 patients on 100 to 600 mg/day (median 300), in 1 patient incessant atrial flutter developed that was relatively refractory to direct-current cardioversion. In 11 patients with atrial fibrillation, sinus rhythm was restored in 7 (after direct-current cardioversion in 3) with doses of 100 to 600 mg/day (median 300) and has been maintained in 5 with associated improvement in symptoms. Despite discontinuation of beta-blocker therapy, chest pain was unchanged in 17 patients, was impaired in 11 and was worse in only 2. Amiodarone was discontinued in 3 patients; in 1 because of hair loss, in 1 because of neurologic symptoms and in 1 because of facial discoloration; in the latter 2 patients, amiodarone was restarted after 1 and 14 months, and was tolerated and effective at the lower dosage.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1984

Arrhythmias in dilated and hypertrophic cardiomyopathy.

The cardiomyopathies are idiopathic muscle disorders that are characterized by hypertrophy, dilation, or restriction. This article discusses arrhythmias in hypertrophic and dilated cardiomyopathy in relation to clinical significance and treatment; when possible, the authors comment on etiology.

Amiodarone↗
PubMed1984

Isovolumic relaxation period in hypertrophic cardiomyopathy.

Previous reports have demonstrated that patients with hypertrophic cardiomyopathy have a prolonged isovolumic relaxation period as a result of a delay in mitral valve opening, reflecting a reduced rate of fall of left ventricular pressure. This period as measured from the aortic closure sound (A2 on phonocardiogram) to the opening of the mitral valve (on echocardiogram) was determined in 84 patients with hypertrophic cardiomyopathy and compared with findings in 31 normal volunteers. The duration of the isovolumic relaxation period in the 84 patients had a wide range from 0 to 160 ms (mean 71 +/- 32) that was not significantly different from that in normal subjects (63 +/- 11 ms). However, it was possible to identify a group of 15 patients with an extremely short isovolumic relaxation period, 2 standard deviations below the normal range. This shortening was due to a marked delay in aortic closure sound (A2) due to late left ventricular-aortic pressure crossover, as well as early opening of the mitral valve secondary to elevated left atrial pressure, which was confirmed by hemodynamic correlations and digitized echocardiographic data. In this subset of patients, A2 is a poor marker of the onset of rapid left ventricular pressure decline and, thus, the interval from A2 to mitral valve opening is not a valid reflection of left ventricular relaxation. It is concluded that in hypertrophic cardiomyopathy, both the timing and sequence of relaxation are abnormal, as is the rate of relaxation. Furthermore, the isovolumic relaxation period is multifactorially determined and depends not only on the rate of left ventricular pressure decline, but also on the magnitude of the pressure drop from A2 to mitral valve opening. All of these determinants must be kept in mind when the isovolumic relaxation period is used as a measure of left ventricular relaxation.

Adolescent↗
PubMed1984

The relationship of myocarditis to dilated cardiomyopathy.

Three patients with congestive cardiomyopathy are reported in whom high neutralizing antibody titres to Coxsackie B viruses were detected. At post-mortem examination, all three had histologically demonstrable chronic inflammation of the myocardium. The hearts of ten patients dying in cardiac failure due to other causes showed no comparable inflammatory infiltration. This provides further evidence that Coxsackie B viral myocarditis is involved in the pathogenesis of some cases of dilated cardiomyopathy. One patient also had pulmonary veno-occlusive disease. This has been reported in association with myocarditis once previously in an infant. A viral aetiology has been postulated. It seems likely in this patient to have also been due to a Coxsackie B virus.

Adolescent↗
PubMed1984

Left ventricular function in patients with ankylosing spondylitis and Reiter's disease.

We have studied left ventricular function by non-invasive methods in 28 patients with ankylosing spondylitis and 14 with Reiter's disease and compared them with 42 normal subjects. A dilated and poorly contracting left ventricle with abnormal systolic time intervals were found in five (18%) of those with ankylosing spondylitis and two (14%) with Reiter's disease. Our results suggest that the high cardiovascular morbidity and mortality in these diseases may be due to abnormality of the myocardium in the absence of valve disease.

Adolescent↗
PubMed1984

Relation between left ventricular gradient and relative stroke volume ejected in early and late systole in hypertrophic cardiomyopathy. Assessment with radionuclide cineangiography.

Hypertrophic cardiomyopathy is characterised by hyperkinetic left ventricular function, but the effect of an outflow tract gradient on the haemodynamics of ejection remains controversial. To determine the functional importance of left ventricular gradients in hypertrophic cardiomyopathy technetium-99m gated equilibrium radionuclide angiography was performed in 18 normal subjects and 57 patients, 26 with and 31 without left ventricular gradients. Time activity curves were generated from list mode data, and the proportion of stroke volume ejected during various phases of systole was computed. The proportion of stroke volume ejected during the initial third, the initial 50%, and the initial 80% of systole was greater in patients with hypertrophic cardiomyopathy than in normal subjects but was identical in patients with and without left ventricular gradients. The duration of systole was similar in the three groups. These findings favour the interpretation that a left ventricular gradient does not represent true obstruction and are consistent with previous observations that clinical features and prognostic indicators do not relate to gradients in this disease.

Adolescent↗