Value of reversed saphenous vein in minimally invasive direct coronary artery bypass graft procedures.

BACKGROUND: Minimally invasive direct coronary artery bypass graft procedures are gaining acceptance for revision as well as primary coronary revascularization. When suitable, the left and right internal mammary arteries are preferred as bypass conduits; in other cases, the greater saphenous vein, used for standard coronary artery bypass graft procedures, may be useful to revascularize coronary artery branches during minimally invasive direct coronary artery bypass graft procedures. METHODS: We used the greater saphenous vein on three occasions during minimally invasive direct coronary artery bypass graft procedures (1) to revascularize the left anterior descending coronary artery by anastomosis to the left axillary artery in the infraclavicular region, (2) as an extension to the left internal mammary artery to reach the left anterior descending coronary artery, and (3) as a bridge from the splenic artery to bypass the distal right coronary artery. RESULTS: Postoperatively, all 3 patients had relief from symptoms of coronary artery insufficiency and none has been readmitted to the hospital with symptoms. Angiography or thallium studies were not performed to confirm graft patency because all patients were elderly and the risks of these procedures were considered to outweigh their potential benefit. CONCLUSIONS: The greater saphenous vein is a potential bypass conduit for use in minimally invasive direct coronary artery bypass graft procedures as well as for coronary artery bypass graft procedures.

Delayed postoperative cardiac tamponade: diagnosis and management.

Symptoms and signs of decreased cardiac output associated with an elevated venous pressure should alert one to the possibility of delayed cardiac tamponade. Enlargement of the cardiothoracic ratio shown by serial roentgenograms and demonstration of significant pericardial effusion by echocardiogram or radionuclide angiocardiography support the diagnosis. Erratic response of the prothrombin time to administration of warfarin and abnormal results of liver function test are additional clues to its diagnosis. Right heart catheterization documents the presence of tamponade and excludes other diagnostic considerations. Operative decompression of the pericardial space can be accomplished by pericardicentesis, subxiphoid pericardiotomy, median sternotomy, or thoracotomy. Hemodynamic observations following the relief of tamponade assure that an adequate therapeutic procedure has been performed.

Cardiac tamponade: hemodynamic observations in man.

Hemodynamic studies were performed before and after pericardiocentesis in 19 patients with pericardial effusion. Right atrial pressure decreases significantly, from 16 +/- 4 mm Hg (mean +/- SD) to 7 +/- 5 mm Hg in 14 patients with cardiac tamponade. This change was accompanied by significant increases in cardiac output (3.87 +/- 1.77 to 7 +/- 2.2 l/min) and inspiratory systemic arterial pulse pressure (45 +/- 29 to 81 +/- 23 mm Hg). The remaining five patients did not demonstrate cardiac tamponade, as evidenced by lack of significant change in these hemodynamic parameters. In all patients with tamponade, right ventricular end-diastolic pressure (RVEDP) was elevated and equal to pericardial pressure; equilibration was uniformly absent in patients without tamponade. During gradual fluid withdrawal in the tamponade group, significant hemodynamic improvement was largely confined to the period when right ventricular filling pressure remained equilibrated with pericardial pressure. In 10 patients with tamponade and pulsus paradoxus, pulmonary arterial wedge pressure (PAW) was equal to pericardial pressure except during early inspiration and expiration when it was transiently less and greater, respectively; however, inspiratory right atrial pressure never fell below pericardial pressure. In these 10 patients, PAW decreased significantly following pericardiocentesis (P less than 0.001). In the remaining four patients with tamponade but without pulsus paradoxus, all of whom had chronic renal failure, PAW was consistently higher than pericardial pressure or RVEDP and did not decrease after pericardiocentesis. These data tend to confirm the hypothesis that in patients with tamponade, the venous pressure required to maintain any given cardiac volume is determined by pericardial rather than ventricular compliance. When pericardial compliance determines diastolic pressure in both ventricles, relative filling of the ventricles will be competitive and determined by their respective venous pressures (pulmonary vs systemic), which vary with respiration and alternately favor right and left ventricular filling. This results in pulsus paradoxus. However, if pulmonary arterial wedge pressure is markedly elevated before the onset of tamponade, as in patients with chronic renal failure, then pericardial compliance may only determine right ventricular filling pressure. In such cases, pulsus paradoxus may be absent.

Surgical treatment of acute aortic regurgitation in infective endocarditis.

During a six-year period 15 consecutive patients with isolated aortic regurgitation due to infective endocarditis were encountered. None had prior significant aortic valve disease. Elective valve replacement was performed in 13 patients; emergency operation was needed in only 1 patient because of intractable pulmonary edema. One patient died suddenly from acute heart block while undergoing medical treatment. Preoperative cardiac catheterization studies in 10 of the 14 patients revealed gross elevations of left ventricular end-diastolic pressure, pulmonary hypertension, depressed cardiac output, and 3 to 4+ aortic regurgitation. There was 1 early and 1 late postoperative death, both due to systemic embolism, yielding an overall surgical mortality of 14%. After a mean follow-up of 18 months, 10 of the 11 patients are in New York Heart Association Functional Class I. Most patients with acute aortic regurgitation secondary to infective endocarditis have clinically observable congestive heart failure and will eventually require valve replacement. If congestive heart failure can be stabilized by a medical regimen, a course of antibiotic therapy can be administered and elective valve replacement can be performed. The time taken for preoperative antibiotic treatment is not associated with irreversible myocardial damage sufficient to influence the results of operation.

Alterations of right ventricular systolic time intervals by chronic pressure and volume overloading.

Right ventricular (RV) systolic time intervals and hemodynamic parameters were determined by micromanometric techniques in 13 subjects with normal right ventricles (NRV). These data were compared to those of 16 patients with pulmonary hypertension (PH) or predominant pressure overloading and 13 individuals with uncomplicated secundum atrial septal defects (ASD) or predominant volume overloading. In PH, the QP2 interval tends to remain within the normal range due to reciprocal changes in isovolumic contraction (ICT) and ejection (RVET) times. Elevations of pulmonary artery diastolic pressure are associated with increases in the mean rate of isovolumic pressure rise (MRIPR) (r = 0.84), but the latter change does not fully compensate for the widened ventriculoarterial diastolic pressure difference and ICT becomes prolonged (P less than 0.001). Factors other than stroke index depression which may contribute to the decreased duration of RVET (P less than 0.001) include tricuspid regurgitation and elevation of pulmonary vascular impedance. In ASD, QP2 is significantly prolonged (P less than 0.025) due to a significant increase in RVET (P less than 0.005). In contrast to NRV, a linear correlation of RVET and stroke index was not present, which suggested an alteration of ejection dynamics in this group. Despite a high incidence of complete or incomplete right bundle branch block the interval from QRS onset to rapid RV pressure upstroke was not prolonged. This is most probably the result of peripheral bundle branch block of genesis of the QRS pattern by right ventricular hypertrophy.

The contribution of tricuspid valve closure to the first heart sound. An intracardiac micromanometer study.

The sound-pressure correlates of the second high frequency component of a split first heart sound (S1) were investigated in 27 patients. An external phonocardiogram was recorded with high fidelity sound and pressure from the left and right atria in 21 patients, from the pulmonary artery in 14 of these, and from the central aorta in 11. In the remaining six patients, high fidelity recordings from the central aorta and right-sided chambers were obtained with an external phonocardiogram. The external component of S1 that coincided with a left atrial C wave and "internal sound" was defined as M1. In those cases where the left atrial pressure was not recorded, this component could be identified by a low frequency transient in the central aortic pressure trace. The other external high frequency component of S1 that was synchronous with a separate right atrial C wave and "internal sound" was defined as T1; with two exceptions, M1 preceded T1. The two exceptions which caused reversal of this order, so that T1 preceded M1, were due to chronic left bundle branch block and mitral stenosis. In both cases, T1 was shown to be distinctly separated from the upstroke of pressure rise in the central aorta. This finding was also demonstrated in three cases of right bundle branch block and one case with aortic valvular disease. The usual asynchrony of ventricular contraction was altered by induction of ventricular premature systoles; the separation of externally identifiable M1 and T1 components and their internal markers was predictably altered by this maneuver. The occurrence of T1 was variable in relation to the upstroke of the pulmonary artery pressure, which suggests that it is not related to pulmonic ejection. It is concluded that micromanometrically recorded right and left atrial C waves can serve as markers for externally recordable M1 and T1 components of the first heart sound. In addition, T1 is frequently an externally recordable and audible event.

Coronary arteritis in systemic lupus erythematosus.

Acute myocardial infarction in systemic lupus erythematosus may be due to an atheromatous or arteritic process. Confirmation of the latter etiology has previously been made only at postmortem examination. A 45-year-old white woman with known systemic lupus erythematosus developed anginal pain and multiple episodes of acute myocardial infarction. During this period, there was serologic but no other clinical evidence of active systemic lupus erythematosus. Serial coronary angiographic studies were strongly suggestive of an arteritic process based upon (1) a saccular aneurysm with no obstructive lesions in a coronary artery supplying an area of recent transmural myocardial infarction and (2) the development of significant obstructive lesions in a previously normal coronary artery over a period of 18 days. This case illustrates the difficulties in distinguishing between atherosclerosis and arteritis using a single coronary angiographic study. The distinction is significant because of the different therapeutic interventions required.

Determinants of variation between Fick and indicator dilution estimates of cardiac output during diagnostic catheterization. Fick vs. dye cardiac outputs.

Simultaneous Fick and duplicate dye cardiac outputs were done in 105 patients with various cardiovascular diseases during routine cardiac catheterization. Dye was injected into the pulmonary artery and sampled from the brachial artery. Nineteen patients had mitral and/or aortic valvular regurgitation. Eighty-four per cent of the duplicate dye cardiac outputs agreed within 10 per cent variation from the line of identity, and 98 per cent were within 25 per cent. There was no systematic difference between the Fick and dye methods. Seventy-five per cent agree within 20 per cent variation from the line of identity. However, individual variation ranged from -27 to +58 per cent. There was, also, no systematic difference between Fick and dye methods either with low cardiac index or valvular regurgitation. Variation between the two methods was less with low cardiac index and greater with higher cardiac index. The variation was not increased in the presence of valvular regurgitation. The variation in the two methods could partly be explained by errors in the measurement of arteriovenous oxygen difference and oxygen consumption. When the injection is made into the pulmonary artery and sampled from the brachial artery, dye outputs are valid irrespective of the level of resting cardiac index and valvular regurgitation as long as there are enough points to draw a straight line from semilogarithmic trace of the descending limb.

Sound pressure correlates of the Austin Flint murmur. An intracardiac sound study.

Mitral valve motion and pressure correlates of the Austin Flint murmur (AFM) were investigated in nine patients with aortic regurgitation using high fidelity catheter tip micromanometers and the mitral valve echocardiogram (MVE). External phonocardiography demonstrated a mid-diastolic murmur (MDM) in eight subjects and a presystolic murmur (PSM) in five. Maximum intensity of both AFM components was found in the left ventricular (LV) inflow tract; the murmur was not recordable in the left atrium (LA). In two patients, an apparent AFM was recorded in the intracardiac phonocardiogram when absent externally. Only one subject had a significant late diastolic "reversed" or LV to LA gradient; in this patient, presystolic mitral regurgitation was shown angiographically but no PSM was present and MVE revealed absence of atriogenic mitral valve re-opening. In two subjects, a PSM disappeared from the external phono when a "reversed" gradient occurred during the diastolic pause following a ventricular premature systole; this LV to LA gradient was associated with diastolic mitral regurgitation recordable in the left atrial phono. In two patients, LV inflow phono showed the MDM to begin 80-120 msec after the aortic second sound and during the D to E phase of the MVE. The rate of early diastolic mitral valve closure in patients (152 +/- 24 mm/sec) was not significantly different from 13 normals (232 +/- 10 mm/sec). With regard to the genesis of the AFM, the present study concludes: 1) diastolic mitral regurgitation plays no role, and 2) antegrade mitral valve flow is required but simultaneous retrograde aortic flow may also be necessary.

Reversibility of left ventricular asynergy by nitroglycerin in coronary artery disease.

To evaluate the potential reversibility of left ventricular asynergy in patients with coronary artery disease, pre- and postnitroglycerin left ventriculography was performed in 32 subjects. In four other subjects left ventriculography was repeated without intervention of nitroglycerin. Changes in ejection fraction and percentage of systolic shortening of three minor axes from the first to the second angiogram were then calculated. Changes were not significant for the myocardial infarction group or for the control group without the intervention of nitroglycerin. Normal left ventricles showed small but significant changes (p less than 0.05). Patients with coronary artery disease but without previous myocardial infarction who demonstrated asynergy in their first angiogram showed three types of response: (1) no significant change (p less than 0.05)-irreversible asynergy; (2) significant change (p less than 0.025) with residual dysfunction-partially reversible asynergy; (3) significant change (p less than 0.001) without residual dysfunction-completely reversible asynergy. It is concluded that postnitroglycerin ventriculography is useful in assessing the reversibility of left ventricular asynergy in patients with coronary artery disease.