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Biomedical subjects

R Jenni

Publications and source records attributed to R Jenni.

At least 217 records · Page 12Linked to original sources
PubMed1990

Quantification of aortic regurgitation with amplitude-weighted mean flow velocity from continuous wave Doppler spectra.

Aortic regurgitant fraction (RFao) was quantified by estimating the ratio of the forward blood flow through the aortic (Qao) and pulmonary (Qp) valve: RFao = 100(Qao - Qp)/Qao. Aortic and pulmonary flow were measured by the systolic time integrals of the amplitude-weighted mean velocity from continuous wave Doppler spectra recorded over the aortic and pulmonary valves. Thus, measurements are independent of the left and right ventricular outflow tract area. In 20 normal subjects, aortic regurgitant fraction ranged between -2.9% and +12.0% (mean +4.3%), the physiologic value being +2%. In 20 patients with pure aortic regurgitation, aortic regurgitant fraction obtained by Doppler spectra (y) was compared with that calculated from biplane left ventriculography and cardiac output determined with the Fick method (x). The correlation was r = 0.94, (SEE = 5.4%, which is 10.6% of the angiography-Fick mean value). The regression line was y = 0.87x + 6.6 (mean y = 51.2%, mean x = 51.1%). It is concluded that determination of aortic regurgitant fraction in pure aortic regurgitation by using the amplitude-weighted mean velocity from continuous wave Doppler spectra is accurate and allows easy noninvasive evaluation of the regurgitant fraction in routine clinical applications.

Adult↗
PubMed1990

Doppler-echocardiographic findings in a patient with persisting right ventricular sinusoids.

The Doppler-echocardiographic features of persisting right ventricular myocardial sinusoids are presented. An 18-year-old patient with persisting right ventricular sinusoids had undergone comissurotomy for critical pulmonary artery stenosis at the age of 12 months. Follow-up catheterization at the age of 17 years revealed no signs of residual pulmonary artery stenosis, outflow tract obstruction or pulmonary hypertension. No shunt could be documented. High systolic velocity jets within the myocardial sinusoids were recorded by means of continuous-wave Doppler. Pulmonary artery blood flow velocity was recorded mainly consequent to atrial contraction and was reduced during right ventricular ejection period, thus reflecting impaired systolic and diastolic right ventricular function.

Echocardiography, Doppler↗
PubMed1990

Dissecting aneurysm of the pulmonary artery with pulmonary hypertension.

Pulmonary artery dissection was observed in a 64-yr-old female patient with severe pulmonary hypertension, which was probably primary (pulmonary vascular resistance, 817 dyn.s.cm-5; normal range less than or equal to 200 dyn.s.cm-5). The patient was admitted to the hospital because of severe dyspnea on exertion. Echocardiography demonstrated a dissecting aneurysm of the pulmonary artery. Right heart catheterization revealed severe pulmonary hypertension (mean pulmonary artery pressure, 64 mm Hg; normal range, 10 to 22 mm Hg); dissection of the pulmonary artery was confirmed by pulmonary arteriography. One-year follow-up was uneventful. In the literature, 28 patients with dissecting aneurysm of the pulmonary artery are reviewed. The dissection has only been diagnosed in life in one patient (by echocardiography).

Aortic Dissection↗
PubMed1990

[Comparison of enalapril and captopril in the treatment of chronic heart failure].

The long-term effect of enalapril (group 1) and captopril (group 2) on clinical symptomatology and left ventricular function was evaluated in 29 patients with severe congestive heart failure (13 ischemic and 12 dilated cardiomyopathy, four valvular heart disease). During the 6-month observation period, five patients died (two on enalapril and three on captopril therapy = 6-month mortality rate 18%). Nine patients showed no beneficial effect of enalapril or captopril on clinical and hemodynamic findings (= nonresponders). The initial findings on these nine patients were, however, not significantly different from the clinical and hemodynamic findings on the patients who improved. Enalapril had to be discontinued in two patients because of side effects (progressive renal failure and gastrointestinal symptoms, respectively). A total of 22 patients completed the study, 11 treated with enalapril (mean dosage 25 +/- 10 mg/day) and 11 treated with captopril (mean dosage 77 +/- 26 mg/day). After 6 months there was a significant improvement according to the New York Heart Association (NYHA) classification, from 2.4 to 1.9 in group 1 (p less than 0.01) and from 2.7 to 1.9 in group 2 (p less than 0.001). The cardio-thoracic ratio (chest x-ray) decreased significantly from 0.59 to 0.56 (p less than 0.001) in group 1 and from 0.56 to 0.53 (p less than 0.001) in group 2. Physical working capacity (bicycle ergometry) showed a significant increase in both groups from 61% to 81% in group 1 (p less than 0.01) and from 66% to 83% in group 2 (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1989

Nifedipine for high altitude pulmonary oedema.

In a laboratory at 4559 m six subjects with high altitude pulmonary oedema (HAPO) characterised by clinical signs, severe hypoxaemia, widened alveolar-arterial oxygen gradient, pulmonary hypertension, and alveolar oedema on chest radiography were treated with nifedipine. Despite continued exercise at the same altitude this treatment, without supplementary oxygen, resulted in clinical improvement, better oxygenation, reduction of alveolar arterial oxygen gradient and pulmonary artery pressure, and progressive clearing of alveolar oedema. Nifedipine offers a potential emergency treatment for HAPO when descent or evacuation is impossible and oxygen is not available. The findings also suggest that hypoxic pulmonary hypertension is essential in the pathogenesis of HAPO.

Acute Disease↗
PubMed1989

[Long-term course of hypertrophic cardiomyopathy: drug versus surgical therapy].

139 patients with hypertrophic cardiomyopathy (HCM) have been followed up for 1-28 years (mean 8.9 years). Group 1 consisted of 60 patients (mean age 38 years) without indication for septal myectomy (SM) (no pressure gradient at rest in 8, pressure gradient less than 50 mm Hg in 52 cases); group 2 consisted of 79 patients (mean age 36 years) who had SM (pressure gradient at rest 70 mm Hg). Management in group 1 was the following: (1a) propranolol (n = 20) (160 mg/d), (1b) verapamil (n = 18) (360 mg/d) and (1c) no therapy (n = 22). 19 patients died in group 1 (mortality 3.6% year); 17 died in group 2 (mortality 2.4%/year). 10 year survival in group 1b was 80% and in groups 1a und 1c 67% and 65% respectively. Patients of group 1b had a higher survival rate (p less than 0.05) than the other subgroups. Surgery patients treated with verapamil (120-360 mg/d) (n = 17) had a 10-year survival rate of 100% compared to 78% for surgery patients (n = 34) without such treatment (p less than 0.05). In summary, it can be said that the overall survival rate after SM is better than that with medical treatment. Under verapamil, however, survival is not different from that after surgery. The most favorable outcome was observed in surgery patients under long-term therapy with verapamil, probably due to the reduction of systolic pressure overload (SM) and improvement in diastolic function (verapamil).

Adult↗
PubMed1989

[Ventricular septal defect following myocardial infarct].

Surgery was performed for postinfarction ventricular septal defect (VSD) in 25 consecutive patients (14 men, 11 women; mean age 68 +/- 8 years). 9 patients were preoperatively in cardiogenic shock and required mechanical circulatory support by intra-aortic balloon pump (IABP) before surgery, whereas 11 acute patients underwent surgery without use of the IABP beforehand. The following procedures were performed: VSD patch closure in 25/25 patients, resection of infarct in 15/25, and patch enlargement of the left ventricle in 3/25. The overall 30-day mortality was 6/25 (24%). However, mortality was higher (4/9 [44%]) in the group with IABP support versus the group of acute patients without it (2/11 [18%]: p less than 0.05). In patients with significant postinfarction VSD, surgical closure appears to be mandatory.

Aged↗
PubMed1989

Progressive dilated cardiomyopathy in a patient with longstanding and complete prednisone-induced hematological remission of idiopathic hypereosinophilic syndrome.

A female patient is described in whom the diagnosis of idiopathic hypereosinophilic syndrome (HES) with heart disease and peripheral neuropathy was made at the age of 32 years. Although prednisone induced a prompt and longstanding complete hematological remission, progressive and eventually intractable heart failure developed, and the patient died 6 years later. Endomyocardial biopsy at diagnosis showed infiltration with intact and disintegrated eosinophils and Charcot-Leyden crystals. Echocardiographic follow-up (including Doppler-Echocardiography) revealed mitral regurgitation with thickening and impaired motility of the posterior mitral leaflet, as well as progressive dilated cardiomyopathy. At autopsy, a diffuse interstitial fibrosis with patchy prominence in an eccentric hypertrophic and highly dilated heart was found. There were no significant endocardial thickening and no mural thrombi. In contrast to the findings of the initial endomyocardial biopsy, autopsy revealed no eosinophilic infiltrate. In this case, eosinophil-induced heart disease manifested as dilated cardiomyopathy, without endocardial fibrosis as originally described by Löffler. We speculate, that eosinophils have been deposited predominantly in the myocard at an early stage of disease, and - activated locally - secreted their granule proteins producing an initial damage to capillary endothelial cells and myocytes. After prednisone-induced clearance of eosinophils from blood and tissues, progressive, self-perpetuating interstitial fibrosis of the myocard and loss of myocytes eventually resulted in end-stage dilated cardiomyopathy.

Adult↗
PubMed1989

Diagnosis of constrictive pericarditis by pulsed Doppler echocardiography of the hepatic vein.

The diagnostic value of hepatic venous flow patterns was evaluated for constrictive pericarditis by pulsed Doppler. A characteristic flow pattern was assumed to be associated with the well-known atrial pressure curve. Thirteen patients with constrictive pericarditis were compared to 13 control subjects and to 25 patients with right ventricular pressure overload including 13 patients with tricuspid regurgitation. The characteristic finding in constrictive pericarditis was a W-wave pattern of flow velocities in the dilated hepatic veins, with abrupt reversal of flow late in systole and diastole before the A wave (100% specificity, 68% sensitivity). This depends, however, on the absence of tricuspid regurgitation (for its systolic component) or fast sinus rhythm (for its diastolic component). Additional diagnostic markers were systolic deceleration time of forward flow (40 to 130 ms) and systolic integral of flow velocities (4.3 to -4.0 cm) (sensitivity and specificity greater than or equal to 92%). In the presence of tricuspid regurgitation, diastolic deceleration time less than 150 ms and diastolic integral of flow velocities less than 6 cm were useful diagnostic signs. If combined, these criteria had 100% sensitivity and specificity for the diagnosis. Thus, pulsed Doppler assessment of flow velocities in the hepatic vein facilitates the diagnosis of constrictive pericarditis in clinical routine, using an auxiliary site with unlimited diagnostic access to the characteristic flow velocity pattern, which reflects right atrial pressure curve and filling abnormalities.

Adolescent↗
PubMed1989

[A pulsating swelling in the neck].

This 56-year-old male patient came to our emergency ward because of a painless pulsation on his left neck. The clinical examination revealed an irregular pulse and a systolic murmur praecordially. In further diagnostic procedures the diagnosis of a severe tricuspidal insufficiency could be confirmed. In the history of the patient there was a motorcycle accident with blunt chest trauma which had to be considered as cause of the lesion.

Atrial Fibrillation↗
PubMed1989

Postinfarction ventricular septal defect--surgical strategies and results.

Twenty consecutive patients with postinfarction ventricular septal defect (VSD) were subjected to surgery: there were 8 females and 12 males with a mean age of 67 +/- 9 years. Nine acute patients developed cardiogenic shock, and intra-aortic balloon pump was started before surgery (with IABP). Eight acute patients showed preoperatively relatively stable hemodynamics, and surgery was feasible without previous use of the intra-aortic balloon pump (without IABP). The interval between myocardial infarction and surgery was 13 days for 17 acute cases. In the group with IABP the interval was 8 +/- 5 days versus 19 +/- 11 days in the group without IABP (p less than 0.025). VSD patch closure was performed in 20/20, resection of infarct in 10/20, transventricular approach without resection of infarct in 3/20, patch enlargement of the left ventricle in 2/20, plicature of an aneurysm in 3/20, aorto-coronary bypass in 10/20 (number of bypasses: 2.1 +/- 1.3) and mitral annuloplasty in 1/20. The perioperative 30 days mortality was 5/20 (25%) for the whole series. In the group with IABP mortality was 4/9 (44%) versus 1/8 (13%) in the group of acute patients without IABP (p less than 0.05). Mean follow-up for the 15 surviving patients was 1.7 +/- 1.0 years. Two patients died during the first year, one of them due to carcinoma. After 1 year, mean NYHA functional class was assessed 1.5 +/- 0.6. One patient showed a residual VSD which was closed surgically. Immediate closure of a postinfarction ventricular septal defect is the therapy of choice of this complication of acute myocardial infarct with a natural history showing an extremely high mortality.

Aged↗
PubMed1989

Determination of the ratio of pulmonary blood flow to systemic blood flow by derivation of amplitude weighted mean velocity from continuous wave Doppler spectra.

Conventional Doppler echocardiographic techniques for the estimation of blood flow ratios depend on the precise measurement of the diameters of the aorta and the pulmonary artery and the mean blood flow velocities in these vessels. A simpler and quicker method is described, based on the calculation of the systolic time integrals of the amplitude weighted mean velocities from continuous wave Doppler spectra within the great arteries. In 30 controls the mean (2 SD) ratio of pulmonary to systemic blood flow averaged 0.952 (0.085). The results of the new technique showed a good agreement with those of quantitative dye dilution and oximetry in 16 patients with intracardiac left to right shunts.

Adolescent↗
PubMed1989

Quantification of mitral regurgitation with amplitude-weighted mean velocity from continuous wave Doppler spectra.

Amplitude-weighted mean velocity from continuous wave (CW) Doppler spectra was used to measure aortic flow (QAo) and left ventricular mitral inflow (QLVin). These flows were used to quantify mitral regurgitation fraction: RFm = (QLVin-QAo).QLVin-1.100(%).QLVin was calculated from the diastolic time integral of amplitude-weighted mean velocity that was derived from CW spectra with the transducer placed in the apical window and the CW beam directed toward the left ventricular inflow tract. QAo was obtained from the systolic time integral of amplitude-weighted mean velocity by using the same apical window and directing the CW beam toward the left ventricular outflow tract. In 20 normal subjects, RFm ranged between -6.2% and +8% (mean, -0.8%). In 25 patients with pure mitral regurgitation, RFm obtained by Doppler (y) was compared with RFm calculated from biplane left ventriculography and the Fick method (x). The correlation was r = 0.96, SEE = 6.1% of the mean or 12% of the angio-Fick mean; the regression line was y = 0.96x + 0.18; mean y = 49%, mean x = 51%. It is concluded that RFm can be determined accurately by using amplitude-weight mean velocities from CW Doppler spectra. The advantages of this method are its independence from the measurement of the left ventricular inflow or outflow tract area.

Adult↗
PubMed1988

Left ventricular systolic series elastic properties in aortic stenosis before and after valve replacement.

In seven patients with aortic valve disease the time course of an auxotonic beat was compared with that of an isovolumetric beat produced by aortic cross clamping during open heart surgery. The rate of systolic stress rise (dS/dt; g.cm-2) of the isovolumetric beat at peak meridional wall stress (Sp; g.cm-2) of the auxotonic beat was determined by tipmanometry and simultaneous sonomicrometry and was found to be 87% of maximum dS/dt. In the second part of the study the stiffness index (k) was calculated in patients undergoing cardiac catheterisation according to: k = 0.87.(max.dS/dt)/Sp.Vcf, where Vcf = normalised midwall circumferential fibre shortening velocity (circ.s-1). In 22 patients, 10 controls and 12 patients with aortic stenosis before (pre) and after (post) valve replacement the systolic stiffness index k (circ-1) was determined using tipmanometry and frame by frame angiocardiography. Muscle fibre diameter and interstitial fibrosis were assessed from left ventricular endomyocardial biopsies. The systolic stiffness index k was 15 circ-1 in controls, 14 in preoperative patients with aortic stenosis and 12 (p less than 0.01 v controls) in postoperative patients. There was a significant correlation between k and muscle fibre diameter (r = 0.55; p less than 0.01) but not between k and interstitial fibrosis or ejection fraction. We conclude that systolic stiffness index k is normal despite marked left ventricular hypertrophy in preoperative patients with aortic stenosis. Following successful valve replacement systolic stiffness index decreased and was significantly lower than in controls. Series elasticity appears to be determined by structures related to the muscle cell rather than to interstitial fibrosis.

Aortic Valve Stenosis↗