Aortic and mitral regurgitation. How to evaluate the condition and when to consider surgical intervention.
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Aortic Valve↗
Biomedical subjects
W Grossman
Publications and source records attributed to W Grossman.
The pacing stress test: a reexamination of the relation between coronary artery disease and pacing-induced electrocardiographic changes.
Electrocardiographic (ECG) changes during graded pacing-induced tachycardia have been considered unreliable as a test for the presence of coronary artery disease (CAD) because of poor sensitivity and specificity. As a result, atrial pacing has not been widely used as an alternative to exercise testing. However, the limited value of the pacing stress test may be related to technical aspects, such as the duration of pacing and ECG monitoring. To study this problem, 22 patients undergoing coronary cineangiography underwent standard exercise stress testing and graded tachycardia induced by atrial pacing. A 12-lead ECG recorder was used for both tests. Pacing tachycardia was terminated when 85% of maximal predicted heart rate had been achieved or when significant ischemic chest pain accompanied by diagnostic ECG changes occurred. The ECG was considered positive if at least 1 mm of horizontal or downsloping ST-segment depression was present. Six patients with normal or minimally diseased coronary arteries were compared to 16 patients with significant CAD. Of the patients without significant CAD, 5 (83%) had a negative electrocardiogram during both exercise and pacing. Of 16 patients with CAD, the electrocardiogram was positive for ischemia in 10 patients (63%) during exercise, in 15 (94%) during atrial pacing and in 12 (80%) after pacing. When the presence or absence of ECG changes was compared between the exercise and the pacing tests, there was a concordance of 90% (Fisher p less than 0.0015). Two patients without significant CAD (33%) had chest pain during both exercise and pacing. Among patients with CAD, 7 (44%) had chest pain during exercise and 8 (50%) had chest pain during atrial pacing.(ABSTRACT TRUNCATED AT 250 WORDS)
Blood Pressure↗
Angina pectoris. Natural history and strategies for evaluation and management.
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Angina Pectoris↗
Left ventricular pressure-volume diagrams and end-systolic pressure-volume relations in human beings.
Assessment of left ventricular pressure-volume relations serially in response to altered loading conditions and heart rate has been difficult to achieve with contrast ventriculography. Accordingly, to study changing pressure-volume relations during altered loading and heart rate, left ventricular pressure and radionuclide absolute volume curves (obtained using a counts-based method with attenuation factor corrections) were recorded in 20 patients. Ventricular pressure and radionuclide volume curves were digitized and synchronized to end-diastole, and pressure-volume plots were subsequently constructed from 32 pressure-volume coordinates throughout the cardiac cycle. In all patients, the correlation between radionuclide absolute volumes and angiographic ventricular volumes was r = 0.92. In 10 patients in whom both radionuclide and angiographic pressure-volume diagrams were constructed, the agreement between the two methods was excellent. With this method, end-systolic pressure-volume relations were examined during altered left ventricular loading conditions, pacing-induced incremental increases in heart rate and pacing-induced ischemia. Using pharmacologically induced changes in left ventricular loading conditions, the slope and volume intercept of the end-systolic pressure-volume line could be calculated as a means of assessing basal contractility. During pacing-induced tachycardia, the slope and volume intercept of the end-systolic pressure-volume line could be calculated to quantify the Treppe effect and assess negative inotropic changes secondary to ischemia. This study supports the validity of using serial recordings of left ventricular pressure and radionuclide volumes to assess left ventricular pressure-volume relations, and indicates that this approach may be useful in the analysis of end-systolic pressure-volume relations in patients.
Cardiac Pacing, Artificial↗
The pacing stress test: thallium-201 myocardial imaging after atrial pacing. Diagnostic value in detecting coronary artery disease compared with exercise testing.
Many patients suspected of having coronary artery disease are unable to undergo adequate exercise testing. An alternate stress, pacing tachycardia, has been shown to produce electrocardiographic changes that are as sensitive and specific as those observed during exercise testing. To compare thallium-201 imaging after atrial pacing stress with thallium imaging after exercise stress, 22 patients undergoing cardiac catheterization were studied with both standard exercise thallium imaging and pacing thallium imaging. Positive ischemic electrocardiographic changes (greater than 1 mm ST segment depression) were noted in 11 of 16 patients with coronary artery disease during exercise, and in 15 of the 16 patients during atrial pacing. One of six patients with normal or trivial coronary artery disease had a positive electrocardiogram with each test. Exercise thallium imaging was positive in 13 of 16 patients with coronary artery disease compared with 15 of 16 patients during atrial pacing. Three of six patients without coronary artery disease had a positive scan with exercise testing, and two of these same patients developed a positive scan with atrial pacing. Of those patients with coronary artery disease and an abnormal scan, 85% showed redistribution with exercise testing compared with 87% during atrial pacing. Segment by segment comparison of thallium imaging after either atrial pacing or exercise showed that there was a good correlation of the location and severity of the thallium defects (r = 0.83, p = 0.0001, Spearman rank correlation). It is concluded that the location and presence of both fixed and transient thallium defects after atrial pacing are closely correlated with the findings after exercise testing.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
The pacing stress test reexamined: correlation of pacing-induced hemodynamic changes with the amount of myocardium at risk.
To assess the relation between extent of ischemia and the magnitude of hemodynamic changes, 25 patients (5 with normal coronary arteries and 20 with significant coronary obstructive disease) were studied with rapid atrial pacing and thallium scintigraphy at the time of cardiac catheterization. Hemodynamic variables were measured before, during and after maximal pacing. Thallium was injected intravenously during maximal pacing and scans in three standard views were obtained immediately in the catheterization laboratory, with delayed scans obtained 4 hours after the cessation of pacing. The three thallium scans were each subdivided into five segments, and a thallium score was obtained on the basis of the total number of segments that were hypoperfused. Each patient was assigned a total thallium score corresponding to thallium defects at maximal pacing, as well as a redistributed thallium score corresponding to the difference between thallium score at maximal pacing and that 4 hours later. With pacing, patients with normal coronary arteries demonstrated no significant change in baseline hemodynamic variables, whereas patients with coronary artery disease exhibited a decrease in cardiac index, an increase in systemic vascular resistance, a widening of arteriovenous oxygen difference, an increase in pulmonary capillary wedge pressure and mean pulmonary artery pressure during maximal pacing and an increase in left ventricular end-diastolic pressure immediately after pacing. There was a significant correlation (Spearman rank r = 0.64, p less than 0.01) between redistributed thallium score and an increase in left ventricular end-diastolic pressure in the postpacing period. Moreover, there was an even higher correlation (Spearman rank r = 0.90, p less than 0.001) between total thallium score and the postpacing increase in end-diastolic pressure. It is concluded that in patients with coronary artery disease the magnitude of pacing-induced hemodynamic changes reflects both the amount of myocardial tissue at ischemic jeopardy and the total mass of hypoperfused myocardium during maximal pacing stress.
Adult↗
Restrictive cardiomyopathy.
Restrictive cardiomyopathy is a descriptive clinical and hemodynamic syndrome emphasizing the pathophysiologic mechanisms by which myocardial hypertrophy and/or infiltrative processes cause cardiocirculatory morbidity. This diagnosis can be made with precision only after pericardial construction is excluded and myocardial biopsy has identified the restrictive process. Though a variety of rather rare infiltrative pathological entities may be responsible for the restrictive cardiomyopathic picture, most commonly no definitive pathologic diagnosis is established despite extensive hemodynamic and histologic investigation. Nonetheless, a therapeutic trial with a calcium entry blocking agent is warranted.
Amyloidosis↗
Instantaneous measurement of left and right ventricular stroke volume and pressure-volume relationships with an impedance catheter.
The feasibility of using continuous on-line recording of intraventricular electrical impedance to measure ventricular stroke volume was assessed in 12 patients at cardiac catheterization with a multielectrode impedance catheter and a 1.3 kHz measuring current of 4 microA. Stroke volumes determined by electrical impedance were compared with stroke volumes determined by the thermodilution technique in 10 patients and correlated with an r value of .95. Directional changes in impedance recordings throughout the cardiac cycle were also compared with volume curves obtained from six patients by radionuclide ventriculography, and in all instances the agreement between the two volume recordings was excellent. For all patients, on-line measurements of impedance showed a beat-by-beat decrease in stroke volume with the Valsalva maneuver and the administration of amyl nitrite, as well as an immediate increase in stroke volume in the contraction following an extra-systolic beat. Similar directional changes in stroke volume were recorded in both left and right ventricles. Left ventricular pressure-volume relationships were assessed with simultaneous left ventricular pressure recordings and volume signals recorded from the impedance catheter to determine if impedance measurements of volume can be used clinically. Pressure-volume diagrams were subsequently plotted, and for all patients these diagrams showed characteristic isovolumetric contraction and relaxation phases as well as typical ejection and filling periods. Moreover, beat-by-beat sequential pressure-volume diagrams constructed for patients during the administration of amyl nitrite revealed a linear end-systolic pressure-volume relationship.(ABSTRACT TRUNCATED AT 250 WORDS)
Blood Pressure↗
Improvement in indexes of diastolic performance in patients with congestive heart failure treated with milrinone.
To elucidate the mechanisms by which the new bipyridine inotropic agent milrinone improves cardiac function, we examined multiple indexes of left ventricular diastolic function before and after administration of milrinone to patients with advanced (NYHA class III or IV) congestive heart failure. In 13 patients left ventricular pressure measurements were made with a micromanometer to permit assessment of peak negative dP/dt and the time constant of left ventricular isovolumic relaxation, T, before and after milrinone. In nine patients radionuclide ventriculographic studies were performed during left heart catheterization, allowing calculation of left ventricular peak filling rate, volumes, and the diastolic pressure-volume relationship before and after milrinone. After intravenous administration of milrinone, peak negative dP/dt increased (+ 18%; p less than .01) and T decreased (-30%; p less than .01), while heart rate increased by only 8% (87 +/- 12 to 94 +/- 15 beats/min; p less than .01), left ventricular systolic pressure did not change, and mean aortic pressure fell by 11% (p less than .01). Left ventricular peak filling rate increased (1.2 +/- 0.6 to 1.7 +/- 0.7 end-diastolic volumes/sec; p less than or equal to .02) despite a decrease in left ventricular filling pressure (mean pulmonary wedge pressure 27 +/- 7 to 18 +/- 9 mm Hg; p less than .01). There was a fall in left ventricular end-diastolic pressure (28.6 +/- 6 to 19 +/- 7 mm Hg; p less than or equal to .01), with no significant change in left ventricular end-diastolic volume. This was associated with a downward shift in the left ventricular diastolic pressure-volume relationship in most cases.(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗
Left ventricular diastolic pressure-segment length relations and end-diastolic distensibility in dogs with coronary stenoses. An angina physiology model.
Isovolumic relaxation abnormalities have been noted in the ischemic left ventricle, but altered end-diastolic distensibility, as well as the role of right ventricular distention, is debated. Accordingly, left ventricular end-diastolic pressure and myocardial segment length were studied in the open-chest dogs with critical (90% diameter reduction) stenoses on both left anterior descending and circumflex coronary arteries. Regional segment length was measured with ultrasonic crystals placed subendocardially, and ischemia was induced by pacing tachycardia for 3 minutes. Transient vena caval occlusion was done to unload the right ventricle and to produce a series of left ventricular end-diastolic pressure and left ventricular end-diastolic segment length points before and after pacing tachycardia. After pacing tachycardia, left ventricular end-diastolic pressure (9.3 +/- 0.9 to 16.9 +/- 1.5 mm Hg, P less than 0.001) and time constant T of left ventricular isovolumic pressure decline (46 +/- 3 to 60 +/- 5 msec, P less than 0.01) increased, with an increase in left ventricular end-systolic segment length (9.8 +/- 0.3 to 10.5 +/- 0.3 mm, P less than 0.001), and a decrease in fractional shortening (17.6 +/- 1.7 to 14.5 +/- 1.3%, P less than 0.01) in the ischemic region, although right ventricular end-diastolic pressure was unchanged. With vena caval occlusion, right ventricular diastolic pressure fell promptly to near zero, followed by decrease in left ventricular pressure and segment length. In each dog, the left ventricular end-diastolic pressure-end-diastolic segment length relation shifted upward after pacing tachycardia. Pacing tachycardia was performed again in six dogs without stenoses. In this group, fractional shortening was preserved after pacing tachycardia (15.7 +/- 2.3 to 15.3 +/- 2.3%, NS), and left ventricular end-diastolic pressure (9.4 +/- 1.8 to 9.8 +/- 1.8 mm Hg, NS) was unchanged. The left ventricular end-diastolic pressure-segment length relation did not shift upward after pacing tachycardia. These data indicate that extrinsic compression of left ventricle by right ventricle is unlikely to be responsible for the upward shift in this model, and the upward shift in end-diastolic left ventricular pressure-segment length relations, as well as dynamic left ventricular diastolic pressure-segment length, supports the concept that persistent myosin-actin interaction throughout diastole plays an important role in the diastolic abnormalities in this angina physiology model.
Angina Pectoris↗
Evaluating the radiographic assessment of pulmonary venous hypertension in chronic heart disease.
This study evaluated how accurately the chest film could be used to determine pulmonary capillary wedge pressure (PCW) in patients with chronic heart disease. Six experienced readers interpreted the erect posteroanterior chest radiographs of 50 patients whose measured PCWs ranged from 6 to 38 mm Hg. Direct numeric estimates of PCW from the films were closely related to measured levels of PCW (r = 0.675). This linear correlation increased to 0.81 when individual-reader variations were reduced by taking a "consensus" (mean) of the six readers' estimates for each case. A combination of the judged degree of pulmonary blood flow redistribution (PFR) and three particular signs of pulmonary venous hypertension (PVH), basal and perihilar vascular blurring and alveolar edema, adequately summarized the radiographic information about PCW. These combined judgments of PFR/PVH identified films from patients with higher and lower PCW levels as accurately as readers' numeric estimates of PCW. Other radiographic signs (enlargement of the heart and central pulmonary vessels and the presence of Kerley lines or pleural effusion) were also positively related to increases in PCW, but added little to the information provided by the PFR/PVH criteria.
Adolescent↗
Clinical use of pressure-dimension and stress-shortening relations in systole and diastole.
The concept of time-varying elastance is an important one and has clinical relevance for both systole and diastole. The application of this concept to systole has permitted the development of end-systolic pressure-volume (dimension) and stress-shortening analysis as a method of assessing myocardial contractility in patients at risk for congestive cardiomyopathy. The application of the time-varying elastance concept to diastole is particularly relevant to new findings concerning abnormal relaxation in hypertrophic cardiomyopathy and angina pectoris.
Adolescent↗
Evaluation of a new bipyridine inotropic agent--milrinone--in patients with severe congestive heart failure.
Milrinone, a derivative of amrinone, has nearly 20 times the inotropic potency of the parent compound and does not cause fever or thrombocytopenia in normal volunteers or in animals sensitive to amrinone. In 20 patients with severe congestive heart failure, intravenous milrinone resulted in significant decreases in left ventricular end-diastolic pressure (from 27 +/- 2 to 18 +/- 2 mm Hg), pulmonary wedge pressure, right atrial pressure, and systemic vascular resistance, as well as a slight reduction in mean arterial pressure. Significant increases occurred in cardiac index (from 1.9 +/- 0.1 to 2.9 +/- 0.2 liters per minute per square meter) and the peak positive first derivative of left ventricular pressure, with a slight increase in heart rate. Hemodynamic improvement was sustained during a 24-hour continuous infusion. Nineteen of the 20 patients subsequently received oral milrinone (29 +/- 2 mg per day) for up to 11 months (mean, 6.0 +/- 0.8), with sustained improvement in symptoms of heart failure. In 10 patients receiving long-term oral milrinone (greater than or equal to 6 months) radionuclide ventriculography showed continued responsiveness, with a 27 per cent increase in left ventricular ejection fraction after 7.5 mg of the drug. Four patients died after a mean of 4.8 months of therapy, and three patients with severe underlying coronary-artery disease and angina pectoris required additional antianginal therapy. No patient had fever, thrombocytopenia, gastrointestinal intolerance, or aggravation of ventricular ectopy. We conclude that milrinone shows promise for the longterm treatment of congestive heart failure.
Administration, Oral↗
Management of adults with congenital bidirectional cardiac shunts, cyanosis, and pulmonary vascular obstruction: successful operative repair in 3 patients.
Patients with congenital cardiac shunts in whom marked functional disability, cyanosis and pulmonary arterial hypertension develop have been considered inoperable or at exceedingly high risk. Three adult patients, 2 with atrial septal defect (ASD) and 1 with patent ductus arteriosus (PDA), presented with New York Heart Association class IV symptoms, bidirectional shunting with cyanosis, polycythemia, severe pulmonary hypertension, and increased pulmonary vascular resistance. Pulmonary arterial pressure did not decrease in response to administration of 100% oxygen in any patient, and 2 had lung biopsy results showing advanced pulmonary vascular obstruction. While a right-to-left shunt caused cyanosis in all patients, the net shunt was left to right (Qp/Qs greater than 1) and the resistance ratio (Rp/Rs) less than 0.5. All 3 patients survived operation, became acyanotic with normal hematocrit, and are in functional class I or II a mean of 36 months postoperatively. At repeat cardiac catheterization, pulmonary arterial pressure and resistance had decreased substantially. This high-risk group of patients with bidirectional shunts, in whom cyanosis due to pulmonary vascular obstruction and polycythemia develop and who appear to be at very high operative risk, should still be considered for surgical correction if the usual criteria for operability exist: net left-to-right Qp/Qs and Rp/Rs less than 0.50.
Adult↗
A catheterization technique for reproduction of a human atherosclerotic lumen within the dog coronary artery in vivo.
Reproduction of a human atherosclerotic lumen within the arterial lumen of an intact animal would facilitate angiographic and hemodynamic studies of stenoses. Accordingly, a male silicone rubber cast of a human atherosclerotic lumen was obtained from a cadaver artery, and a thin-walled replicate arterial phantom was constructed from the cast by use of a rapidly polymerizing liquid plastic. The casting properties of both materials were such that the topography of the arterial lumen was duplicated precisely in the phantom with 20 x microscopic detail preserved. The phantom was coated with a banzalkonium-heparin solution and introduced over a guidewire into an epicardial segment of a coronary lumen of the dog. Similarly, a larger phantom was placed within the dog femoral artery either directly via an arteriotomy or indirectly via a catheterization technique. Since the plastic material used to make a phantom had the same radiographic density of tissue, the angiographic appearance of an intra-arterial phantom was that of a human stenosis.
Animals↗
Right ventricular function in adults with pulmonary hypertension with and without atrial septal defect.
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Adult↗
In vivo coronary angioscopy.
The feasibility of in vivo coronary angioscopy was tested utilizing a 1.8 mm angioscope in vessels where blood had been replaced by optically clear liquids, including a new perfluorocarbon emulsion. After trials in postmortem canine and human coronary arteries, in vivo intraluminal visualization was accomplished in the dog with a catheterization technique and in patients during open heart surgery. The results demonstrate the feasibility and potential clinical usefulness of direct visualization of intravascular anatomy and disease, analogous to endoscopy of other organ systems.
Animals↗
Comparison of the effects of nitroprusside and nifedipine on diastolic properties in patients with hypertrophic cardiomyopathy: altered left ventricular loading or improved muscle inactivation?
The calcium channel blocking agent, nifedipine, has been shown to improve indexes of left ventricular relaxation, diastolic filling and compliance in patients with hypertrophic cardiomyopathy. The mechanism of action of nifedipine on diastolic properties in patients with hypertrophic cardiomyopathy is unclear and could result from an improvement in myocardial inactivation or from systemic vasodilation and left ventricular unloading. To distinguish between these mechanisms, the effects of nifedipine and the vasodilator nitroprusside on left ventricular diastolic properties were compared in 10 patients with nonobstructive hypertrophic cardiomyopathy using simultaneous micromanometer left ventricular pressure and echocardiographic measurements. Left ventricular peak systolic pressure was comparable during nitroprusside infusion (132 +/- 38 mm Hg) and after nifedipine (132 +/- 32 mm Hg). During nitroprusside infusion, the decrease in left ventricular end-diastolic pressure (22 +/- 11 to 17 +/- 11 mm Hg, p less than 0.05) was associated with a decrease in left ventricular end-diastolic dimension. In contrast, the decrease in left ventricular end-diastolic pressure after nifedipine (22 +/- 11 to 18 +/- 10 mm Hg, p less than 0.05) was associated with no reduction of left ventricular end-diastolic dimensions, suggesting an increase in left ventricular distensibility. Compared with nitroprusside, nifedipine was associated with less prolongation of the left ventricular isovolumic relaxation time and less depression of the peak left ventricular posterior wall thinning rate and peak left ventricular internal dimension filling rate. These data suggest that the effects of the calcium channel blocker, nifedipine, on diastolic mechanics in hypertrophic cardiomyopathy result not only from systemic vasodilation but also from improved cardiac muscle inactivation.
Adolescent↗