Ear oximetry: a noninvasive method for detection of patent foramen ovale: a study comparing dye dilution method and oximetry with contrast transesophageal echocardiography.

BACKGROUND AND PURPOSE: Patent foramen ovale (PFO) may play an important role as a risk factor for ischemic stroke and some other neurological conditions. There is a need for low-cost and noninvasive methods for the detection of PFO. This study evaluates the accuracy of two simple bedside tests, the dye dilution method and ear oximetry, in the detection of PFO. METHODS: Dye dilution curves and ear oximetry recordings with a noninvasive ear densitometer were obtained from consecutive cryptogenic stroke patients referred for contrast transesophageal echocardiography (TEE). All test results were blindly assessed for the presence of PFO. Sensitivity and specificity were calculated with TEE used as a reference method. kappa statistics were used to measure interrater agreement. RESULTS: Dye dilution curves were obtained from 67 patients. Dye dilution correctly diagnosed 35 of the 46 patients who had PFO in TEE and all the 21 patients without PFO. Thus, the sensitivity (95% CI) of the dye dilution method was 76% (61% to 87%) and its specificity 100% (84% to 100%). Ear oximetry was done on 83 patients. Oximetry correctly diagnosed 45 of the 53 patients who had PFO in TEE and all of the 30 patients without PFO. Thus, the sensitivity of ear oximetry was 85% (72% to 93%) and its specificity 100% (88% to 100%). The interrater agreement was excellent (kappa value 0.94 for dye dilution and 0.90 for oximetry). CONCLUSIONS: Dye dilution and oximetry are both sensitive and specific methods for the detection of PFO. Oximetry has the following primary advantages over the currently available diagnostic methods: it is noninvasive, safe, and inexpensive and causes no discomfort for the patient. We suggest that oximetry could be used as a first-line screening method for PFO in patients with cryptogenic stroke. Ear oximetry also has potential use in epidemiological studies.

Dye dilution and oximetry for detection of patent foramen ovale.

OBJECTIVES: Patent foramen ovale (PFO) is a risk factor for stroke of undetermined (cryptogenic) origin. Low cost and non-invasive bedside tests for detection of PFO are needed as alternatives to contrast transesophageal echocardiography. We investigated whether dye dilution curves and oximeter recordings are useful for detecting PFO and what is the prevalence of PFO in patients with cryptogenic stroke determined with these bedside methods. We also studied whether stroke risk factors, number of brain lesions, and stroke recurrence rates were different in patients with an unexplained stroke with and without PFO. MATERIAL AND METHODS: Dye dilution curves and oximeter recordings with non-invasive earpiece apparatus were obtained in 59 patients aged under 50 years who had had a cryptogenic brain infarction. The number of ischemic lesions in the brain was counted by MRI. RESULTS: PFO was found in 24 (41%) of 59 patients. There was a 100% concordance in results obtained by dye dilution and by oximetry. Risk factors for stroke were similar in subjects with PFO and those without PFO. No significant association was found between PFO and Valsalva-like activity at stroke onset. Those with PFO did not have more ischemic lesions detected by MRI nor did they have more recurrent ischemic episodes. CONCLUSION: Dye dilution and oximetry are cheap and useful methods for detection of PFO and could be used for screening of the risk of paradoxical embolism. Because these 2 methods were not compared with the golden standard, transesophageal echocardiography, the specificity and sensitivity of the tests remain unsettled.

Circadian variation of left ventricular diastolic function in healthy people.

AIM: To assess whether left ventricular function shows circadian variation in healthy people. SUBJECTS AND METHODS: 10 healthy men (7) and women (3) aged 35-50 underwent M mode echocardiography of the left ventricle and Doppler velocimetry of transmitral flow at 4 h intervals over 24 h. The participants were in hospital over the study period and their diet, meal times, and sleeping hours were standardised as far as possible. MEASUREMENTS: Heart rate, blood pressure, left ventricular and atrial diameters, fractional shortening, peak early and late transmitral velocities, time from the second heart sound to the early diastolic velocity peak (relaxation time), isovolumic relaxation period, acceleration and deceleration of the early transmitral flow, atrial filling fraction. RESULTS: A circadian rhythm was observed in heart rate and blood pressure, but neither the left ventricular diameters and systolic function nor the left atrial size showed statistically significant diurnal trends. The relaxation time (mean (SD)) measured 144 (16) ms at 2 pm, 144 (21) ms at 6 pm, 149 (22) ms at 10 pm, 168 (23) ms at 2 am, 174 (28) ms at 6 am, and 151 (21) ms at 10 am (P = 0.009). Diurnal rhythms were seen also in the isovolumic relaxation period (P = 0.003) and in the acceleration of the early diastolic transmitral flow (P = 0.037); the lowest and highest values of flow acceleration were observed during the nocturnal and daytime hours, respectively. CONCLUSIONS: The Doppler indices of left ventricular filling in healthy people show diurnal changes suggestive of a circadian rhythm in the rate of left ventricular relaxation. The most likely underlying mechanism is the day-night cycle in sympathoadrenal activity.

Breath acetone in congestive heart failure.

To summarize, CHF predisposes to postabsorptive ketosis in relation to the severity of venous congestion. A simple and fully noninvasive measurement of breath acetone may add to the diagnostic assessment of patients with CHF.

Influence of negative intrathoracic pressure on right atrial and systemic venous dynamics.

To investigate the effect of a sustained fall in intrathoracic pressure (Mueller manoeuvre) on blood flow through the right heart and on systemic venous dynamics, 16 patients were studied using thermodilution, cinevenograms and simultaneous pressure recordings with two micromanometric transducers. The reductions in airway pressure (median [range]) during two graded Mueller manoeuvres were 25 (20-30) and 42 (22-52) mmHg. Right atrial mean pressure decreased by 17 (2-25) mmHg during the former and 38 (0-49) mmHg during the latter, and simultaneously, pressure gradients of 23 (1-32) and 45 (1-82) mmHg developed between the inferior vena cava and right atrium (P < 0.003 for all). Internal jugular venous pressure decreased by 16 (4-25) and 24 (4-43) mmHg (P < 0.03 for both), respectively, and no pressure gradient developed between internal jugular and superior caval veins. The minimum diameter of the proximal inferior vena cava decreased by 69 (-49-84)% (P = 0.002) during the greater manoeuvre. Cardiac index tended to increase by 26 (-17-40)% (P < 0.066) during the lesser manoeuvre but did not change statistically significantly during the greater. In conclusion, during negative intrathoracic pressure caused acutely by the Mueller manoeuvre, right atrial pressure decreases and the inferior vena cava collapses partially at or below the diaphragm. Despite a significant venous obstruction between the lower body and right atrium, blood flow through the right heart increases or remains constant.

Effect of negative intrathoracic pressure on left ventricular pressure dynamics and relaxation.

To investigate the effect of a fall of intrathoracic pressure on left ventricular (LV) hemodynamics and relaxation, simultaneous micromanometric recordings of LV and aortic pressures were performed at rest and during two graded Mueller maneuvers in 16 patients undergoing cardiac catheterization for aortic valve stenosis (n = 8) or chest pain (n = 8). The reductions (means +/- SE) of airway pressure during the lesser and greater maneuvers were 26 +/- 1 and 42 +/- 1 mmHg, respectively. Simultaneously, LV isovolumic-developed pressure increased by 9 +/- 3 and 21 +/- 4 mmHg, respectively (P < 0.03 for both). During the greater maneuver, the individual changes of the time constant of LV isovolumic relaxation (tau) correlated with the changes of LV isovolumic-developed pressure (r = 0.73; P = 0.002). In patients with a > 20-mmHg rise in isovolumic-developed pressure, tau increased by 10.3 +/- 4.6 ms. By multiple-regression analysis, the change of tau was related directly to the change of isovolumic-developed pressure (standardized coefficient beta = 0.80; P = 0.001) and inversely related to the resting systolic LV-aortic pressure gradient (beta = -0.37; P = 0.050). The other hemodynamic changes were independent of aortic valve stenosis. In conclusion, during the Mueller maneuver, the LV isovolumic contraction load increases and tau lengthens, particularly with higher elevations of LV systolic load.

Atrial septal defect blunts the impairment of left ventricular function during the Mueller maneuver.

To investigate whether atrial septal defect (ASD) modifies the left ventricular (LV) hemodynamic response to a fall of intrathoracic pressure (Mueller maneuver), we studied 15 patients with an uncomplicated ASD and 16 healthy control subjects. LV function was measured by M-mode and Doppler echocardiography at rest and during the maneuver. Indicator-dilution technique was used to quantify the pulmonary-to-systemic flow ratio. During comparable changes (means +/- SE) of intrathoracic pressure (-33 +/- 2 mmHg in persons with ASD vs. -34 +/- 2 mmHg in those without), LV systolic function and filling diminished in both groups but patients with ASD showed smaller reductions in LV stroke dimension (-0.9 +/- 0.5 vs. -2.5 +/- 0.4 mm; P = 0.016), peak diameter shortening rate (-4 +/- 2 vs. -12 +/- 2 mm/s; P = 0.007), transmitral velocity-time integral (-1.0 +/- 0.3 vs. -2.2 +/- 0.4 cm; P = 0.022), and cardiac output (-6 +/- 3 vs. -18 +/- 3%; P = 0.029). The pulmonary-to-systemic flow ratio increased from 2.1 +/- 0.1 to 2.6 +/- 0.2 in the ASD group (P = 0.014). In conclusion, LV function diminishes significantly in healthy persons during the Mueller maneuver. In patients with ASD, the changes are directionally similar but quantitatively smaller. An interatrial communication mitigates the impairment of LV function after an acute and sustained drop of intrathoracic pressure.

Age-dependent influence of heart rate on Doppler indexes of left ventricular filling.

BACKGROUND AND OBJECTIVE: The Doppler indexes of left ventricular filling are related to age and heart rate. The aim of this study was to assess whether the influences of heart rate and age interactions (that is, whether the effect of heart rate on the Doppler indexes) is modified by age. SUBJECTS AND METHODS: The effects of atropine-induced heart rate increases on the transmitral velocities were compared in 10 younger healthy subjects aged 26-38 years and 12 older healthy subjects aged 50-67 years. RESULTS: With a comparable total rise in heart rate (on average 20 beats min-1), the peak early diastolic velocity decreased likewise in both groups (from 66 +/- 9 to 57 +/- 9 cm s-1 in the younger age group and from 58 +/- 15 to 47 +/- 13 cm s-1 in the older age group). The peak atrial velocity remained unaltered in the older group (53 +/- 16 vs. 52 +/- 14 cm s-1) but rose from 33 +/- 6 to 44 +/- 12 cm s-1 in the younger (P = 0.02). The early-to-atrial peak velocity ratio decreased from 1.2 +/- 0.6 to 1.0 +/- 0.4 cm s-1 in the older subjects and from 2.0 +/- 0.5 to 1.4 +/- 0.5 cm s-1 in the younger subjects (P = 0.01). Changes in the other Doppler indexes were similar in both groups. CONCLUSIONS: The effect of heart rate on certain Doppler indexes of left ventricular filling is age-dependent. The peak velocity ratio cannot be interpreted without adjusting for heart rate in younger subjects, whilst in older people heart rate variation is of less importance.

Factors influencing Doppler indexes of left ventricular filling in healthy persons.

Ninety-three healthy persons aged 11 to 91 years were studied to assess the factors influencing Doppler indexes of left ventricular (LV) diastolic filling. The effects of physical activity, alcohol consumption and smoking were tested in addition to those of age, sex, heart rate, body mass index, blood pressure, left atrial diameter, and LV end-diastolic diameter, wall thickness, mass and fractional shortening. The data were fitted stepwise into multiple linear regression models both in the total population and in 3 groups aged less than 40, 40 to 60 and greater than 60 years. In the total population, age explained 45 to 68% of the variation in the peak early and late diastolic velocities, their ratio, deceleration of the early velocity, atrial filling fraction and peak filling rate normalized to mitral stroke volume. With advancing age--and with increases in either body mass index, heart rate, diastolic blood pressure or LV mass--the indexes of early filling decreased, whereas with regular modest use of alcohol or regular aerobic exercise they increased (p less than 0.05 for all). In the middle-aged subjects, gender explained 32 to 57% of the variation in the peak atrial velocity, early to atrial peak velocity ratio and atrial filling fraction; the peak velocity ratio measured 1.4 +/- 0.3 (mean +/- standard deviation) in men vs 1.0 +/- 0.2 in women (p less than 0.001). In conclusion, many constitutional and physiologic factors and even life-style can influence the Doppler indexes of LV filling. This demonstrates the exquisite sensitivity of the method but indicates also that individual measurements must be interpreted with caution.

Left ventricular filling impairment in asymptomatic chronic alcoholics.

Systolic left ventricular dysfunction is relatively common in even asymptomatic alcoholics, but whether diastolic function is also altered is much less well-studied. We used M-mode and Doppler echocardiography to study left ventricular size, mass, systolic function and diastolic filling in 32 alcoholics free of clinically detectable heart disease and in 15 healthy control subjects. Left ventricular mass index and posterior wall thickness were higher in alcoholics than in controls, but there was no statistically significant difference either in end-diastolic size or in systolic ventricular function. More abnormalities were found in the Doppler indexes of diastolic function, however. The alcoholics had a prolonged relaxation time (200 +/- 6 vs 184 +/- 5 ms [mean +/- standard error], p less than 0.05), a decreased peak early diastolic velocity (52 +/- 2 vs 60 +/- 3 cm/s, p less than 0.05), a slower acceleration of the early flow (410 +/- 18 vs 552 +/- 43 cm/s2, p less than 0.01), and a higher atrial-to-early peak velocity ratio (0.74 +/- 0.04 vs 0.60 +/- 0.05, p less than 0.05). This pattern of changes suggests a primary abnormality in the relaxation of the left ventricle. In multivariate analyses, the abnormalities in the Doppler indexes were independent of the duration of alcoholism, the quantity of the most recent ethanol exposure and the increased mass of the left ventricle. Impaired early filling of the left ventricle due to delayed relaxation is common in asymptomatic alcoholics and may in fact be the earliest functional sign of preclinical alcoholic cardiomyopathy.

Acute effects of ethanol on left ventricular diastolic function.

Transmitral flow velocities were measured by Doppler echocardiography in nine healthy men who ingested 1 g/kg of ethanol within one hour. The measurements were made before the first drink and every hour thereafter for three hours. The peak mean (SE) blood ethanol concentration was 21.4 (1.0) mmol/l. Each man was also studied after drinking fruit juice. Ethanol increased the heart rate but did not change the peak transmitral velocities, the normalised peak filling rate, the deceleration of early flow, or the duration of relaxation as measured from the second heart sound to the peak early diastolic velocity. The ratio of the peak atrial to the peak early diastolic velocity rose from 0.41 (0.03) to 0.44 (0.03) after ethanol but remained unchanged after juice. The difference between juice and ethanol was independent of changes in heart rate. The fluid balance was more negative in the ethanol experiment (-727 (114) ml v -107 (70) ml), suggesting a reduction in preload, and the ethanol-induced net loss of fluid correlated with the concomitant change in the velocity ratio. A moderate dose of ethanol causes a small acute increase of the ratio of the peak atrial to the peak early diastolic velocity of mitral flow in healthy subjects. Although this change indicates altered diastolic function of the left ventricle, most of it may result from the diuretic effect of ethanol. Any major impairment of ventricular relaxation seems unlikely.

Early and late results of surgery for atrial septal defect in patients aged over 60 years.

To assess the risks and benefits attending the surgical repair of atrial septal defect in the elderly the case histories of all patients operated on at the age of 60 years or more were reviewed and follow-up study, including cardiac catheterization, was performed. A total of 17 patients (12 females and 5 males) were identified. The left-to-right shunt ratio averaged 2.7. Fifteen patients had abnormally high systolic (greater than 30 mmHg) or mean (greater than 20 mmHg) pulmonary artery pressure and the pulmonary arterial resistance was elevated (greater than 1.5 units) in eight. One patient died shortly after surgery (operative mortality, 6%) and major postoperative complications were found in four additional patients (24%). Three months after surgery the effort capacity had improved by at least one class in all survivors. After an average of 8.2 years follow-up 12 patients were alive. Ten of them felt better than preoperatively. Eight agreed to cardiac catheterization. The pulmonary blood flow was markedly decreased in all (means, 5.6 l/min postoperatively, vs 11.2 l/min preoperatively) even though a hemodynamically significant shunt persisted in two patients. The mean pulmonary artery pressure had decreased in all who were hypertensive before operation (mean, 25 mmHg vs 33 mmHg). It had slightly increased in patients who had normal pulmonary pressure preoperatively (mean, 27 mmHg vs 19 mmHg). The pulmonary arterial resistance was higher than before surgery in all except one patient (mean, 2.2 units vs 1.5 units).(ABSTRACT TRUNCATED AT 250 WORDS)

Ruptured aneurysm of sinus of Valsalva. Long-term postoperative follow-up.

Ruptured sinus Valsalva aneurysm was repaired in 13 patients (mean age c. 33 years). Dyspnea, chest pain, fatigue and palpitation were the most common symptoms and systodiastolic murmur, cardiomegaly and pulmonary congestion the most pertinent clinical findings. The pulmonary-to-systemic flow ratio averaged c. 2.5. Associated cardiac anomalies were ventricular septal defect, aortic or mitral regurgitation, aortic coarctation or subvalvular stenosis, tetralogy of Fallot (altogether 8 cases). The origin of the fistula was the noncoronary, right coronary or left coronary sinus (5, 4 and 3 cases) or was not identifiable (1 case). Rupture occurred into the right atrium (6 cases), right ventricle (6) or pulmonary artery (1 case). Repair was undertaken through aortotomy (6 cases), right ventriculotomy (2) or right atriotomy (1) or through aortotomy + right ventriculotomy or atriotomy (4). In one case aortic valve replacement was performed. All survived the operation. Follow-up averaged 9.6 years. Recurrent fistulation, though with small shunt, was found in two cases. Combined two-dimensional and Doppler echocardiography revealed minor cardiac abnormalities in most patients, particularly aortic regurgitation. All the patients were in NYHA function class I or II.

Prolonged survival with a thrombotically occluded tricuspid valve prosthesis.

A 49-year-old man who had undergone tricuspid valve replacement with a Björk-Shiley prosthesis in November 1974 was reoperated on in January 1985 due to prosthesis malfunction. The operation revealed a totally occluded prosthetic valve and a paravalvular defect which had served as the channel for atrioventricular blood flow. In retrospect, all evidence indicated that the valve had stuck as early as six months after the primary operation, when the patient had first noticed the loss of audible valve clicks and the reappearance of effort intolerance. Due to the gradual progression of the patient's symptoms and misinterpretation of the significance of absent valve clicks, the correct diagnosis was not made until a follow-up study 10 years after the first operation when contrast echocardiography showed the absence of both disc movements and transvalvular contrast flow. Our experience indicates that thrombosis of a tricuspid valve prosthesis may present highly insidiously and that the loss of audible valve clicks should be relied on as a sign of prosthesis malfunction.

Failure of mechanical valves in Ebstein's malformation.

Five patients with Ebstein's malformation were operated on with closure of the atrial septal defect and implantation of a mechanical prosthesis at the right atrioventricular junction. The 4 patients who survived showed an excellent early recovery. Three of the patients noticed the disappearance of the valve clicks 6 months after the operation. At re-examination using echophonocardiography, peripheral dye dilution curves and catheterization, these valves were found to be stuck in the open position in 2 patients and in the closed position in 1 patient. The last patient had a paravalvar channel supplying blood into the right ventricle. One patient who had a St. Jude prosthesis was doing excellently 4 years postoperatively and the valve was functioning well. Two years after the operation, the other patient with a St. Jude valve again noticed valve clicks after over 1 year of silence. Examination revealed the prosthesis to be functioning normally. The totally occluded Björk-Shiley prosthesis (10 years postoperatively) was excised at re-operation and replaced by an Ionescu-Shiley bioprosthesis. The patient with a jammed Björk-Shiley prosthesis (10 years postoperatively) declined a re-operation and is doing well, albeit under close observation.

Auscultatory and echophonocardiographic characteristics of the normally functioning Medtronic-Hall aortic valve prosthesis.

We recorded auscultatory and echophonocardiographic findings in 30 patients who had a normally functioning Medtronic-Hall (M-H) tilting disc valve prosthesis in the aortic position. The opening and closing sounds were invariably audible. Echophonocardiography showed that a typical opening sound consisted of 2 or 3 sharp clicks which were related to the onset and termination of the disc opening excursion. The closing sound comprised at least 2 separate clicks which coincided with the onset and completion of the valve closure. An early systolic ejection type murmur was heard in 25 patients and a faint early diastolic murmur in 2. The disc motion could be recorded echocardiographically in 27 patients. The opening amplitude of the disc varied from 3 to 11 mm. The intervals from the Q wave and the first heart sound to the onset of valve opening measured 116 +/- 20 ms (mean +/- standard deviation) and 54 +/- 14 ms, respectively. The opening and closing velocities of the disc were also easily measurable but showed a wide patient-to-patient variation. In 5 patients, the examination was repeated after 8 to 12 months. The reproducibility was excellent for the auscultatory findings and fair for the echophonocardiographic time intervals and disc opening amplitude, but poor for the disc velocities. Familiarity with these normal findings should help clinicians to determine whether an aortic M-H valve functions normally or not.