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Background Effusive–constrictive pericarditis is an uncommon pericardial syndrome characterized by concomitant tamponade, caused by tense pericardial effusion, and constriction, caused by the visceral pericardium. We conducted a prospective study of its clinical evolution and management. Methods From 1986 through 2001, all patients with effusive–constrictive pericarditis were prospectively evaluated. Combined pericardiocentesis and cardiac catheterization were performed in all patients, and pericardiectomy was performed in those with persistent constriction. Follow-up ranged from 1 month to 15 years (median, 7 years). Results A total of 1184 patients with pericarditis were evaluated, 218 of whom had tamponade. Of these 218, 190 underwent combined pericardiocentesis and catheterization. Fifteen of these patients had effusive–constrictive pericarditis and were included in the study. All patients presented with clinical tamponade; however, concomitant constriction was recognized in only seven patients. At ca...

Background: The use of anticoagulant therapy in patients with infective endocarditis (IE) is a controversial issue. Objective: To study the impact of anticoagulant therapy on the clinical outcome, mortality, and cause of death in a series of patients with native and prosthetic leftsided Staphylococcus aureus IE. Methods: This report is based on all consecutive cases of IE diagnosed at our hospital between 1975 to 1997. Clinical data, including the use of anticoagulant therapy at the time of diagnosis, were prospectively obtained, and antibiotic treatment and surgical indications were uniform throughout the study period. Computed tomographic scans of all clinical records were reviewed. Results: Of 637 consecutive patients with IE, 56 had leftsided S aureus IE affecting native valves in 35 patients and prosthetic valves in 21 patients. Of the patients with prosthetic valve IE, 19 (90%) were taking oral anticoagulant therapy at the time of diagnosis while no patient with native valve IE was receiving such treatment. There were no differences between native valve IE and prosthetic valve IE in age, sex, embolic episodes, and number of central nervous system complications. Mortality was higher in prosthetic valve IE than in native valve IE (71% vs 37%; P = .02). No patient with native valve IE died due to central nervous system complications, while 73% (11 of 15 patients) with prosthetic valve IE died due to central nervous system complications. The difference in the distribution of the type of death (stroke vs other) was significant (P,.007). Conclusions: Our results suggest that in left-sided S aureus IE anticoagulant therapy is closely associated with death due to neurologic damage. According to our data, as soon as the clinical diagnosis of S aureus IE is indicated the use of anticoagulant therapy should be immediately stopped until the septic phase of the disease is overcome. Arch Intern Med. 1999;159:473-475

Coronary ligature with minimal intimal injury reproduces only in part acute coronary syndrome, in which reperfusion occurs through an extensively damaged artery. To analyze the influence of coronary endothelial injury (El) on PMN leukocyte accumulation and infarct size, 48 pigs were allocated to catheterization and endothelial denudation of the LAD or to no intervention immediately before a 48 min coronary occlusion and 6 h of reperfusion. Ninety min before they had received aspirin (ASA, 250 mg e.v.), or placebo (2 × 2 factorial design). Twelve animals presented reocclusion and were excluded for subsequent analysis, 2 of them receiving ASA and 10 not (p l 0.05). In the remaining pigs, blood flow (ml/[min.g]) in the area at risk was similar in those with than in those without EI. 30 min (2.2 ± 0.3 vs 2.3 ± 0.4) and 5 h (1.4 ± 0.2 vs 1.4 ± 0.2) after reflow. and was not modified by ASA. Infarct size (% of the area at risk, TIC reaction) was greater in pigs with EI. A significant interaction (p = 0.03) between El and ASA was detected, El being associated with larger infarcts in animals receiving placebo, but not in those receiving ASA: No EI (n = 18) EI (n = 18) p value Placebo (n = 18) 11 ± 4 36 ± 7 0.006 ASA (n = 18) 22 ± 6 20 ± 6 NS Myocardial content of PMNs (quantitative histology) in the area at risk was higher in animals with than in those without El (mean scores 4.9 ± 0.6 vs 3.0 ± 0.6, p = 0.04), and was not modified by ASA. In 12 additional experiments with 30 min coronary occlusion (no infarct), the content of Tc99 labeled PMNs in the area at risk was significantly increased in pigs with El (144 ± 23% of control myocardium), but not in those without (p = 003). Thus, El at the site of a transient coronary occlusion increases myocardial PMN content and necrosis. ASA reduces reocclusion rate and limits the deleterious effect of EI on infarct size in animals without reocclusion. This effect could be due to impared PMN-platelet cooperation, or to a direct effect of ASA on function of adhered PMNs.

Echocardiographic characteristics of the interventricular septum (IVS) have been studied in eight patients with chronic constrictive pericarditis (CP). Values of septal thickening (ST) were clearly below normal in all cases. Interventricular septal systolic motion (IVSSM) was normal in four cases, hypokinetic in three and paradoxical in one. In seven out of the eight patients, an early interventricular septal diastolic motion (IVSDM) consisting of a sudden anterior displacement followed by a brisk posterior rebound was recorded. The beginning of this anomalous movement was coincident with the pericardial knock in the phonocardiogram and its peak was coincident with the simultaneously recorded deep "y" trough in the jugular pulse tracing. The tendency toward normality of IVSDM observed after pericardiectomy in six out of seven patients suggests that this peculiar interventricular septal systolic motion may be a frequent and probably specific echocardiographic finding in constrictive pericarditis.

A report is given of 13 patients with late prosthetic valve endocarditis (1975-1982). Follow-up ranged from 1 to 8 years (mean 33 months). Causative organisms were streptococci in 8 cases, staphylococci in 2, and Cardiobacterium hominis in 1. Cultures were negative in 2. Surgical treatment in the acute phase was performed in 3 patients. At the latest clinical control, 3 patients had died and 10 patients were asymptomatic, 3 of them having required late operation. These fair results are attributable to the particular spectrum of causative organisms and to the proper timing of surgical treatment in the 3 patients operated during the acute phase.

To determine the electrophysiologic effects of stellate ganglion (SG) block on the human heart, the two SGs were anesthetized separately, with a 24-hour interval between the two procedures, in 13 patients with episodes of supraventricular tachycardia (six had Kent bundles). Left SG block caused: (1) a lengthening of the AH interval, measured at fixed atrial rates of 10 +/- 12 msec (p less than 0.01); (2) a marked depression of the VA conduction in six of the seven patients with measurable VA interval (in two patients it produced complete VA block); (3) a slowing of 20 to 40 msec of the cycle of an electrically induced reciprocating tachycardia; and (4) failure to modify the QT interval duration. In contrast, right SG block produced asymmetric or opposite changes and prolonged the QT interval (7.6 +/- 8.8 msec, p less than 0.05). Atrial and ventricular refractoriness was not significantly altered by SG block. Retrograde effective refractory period of the Kent bundle changed 20 to 60 msec after unilateral SG blockade. Thus, this study suggests that the human conduction system and the Kent bundles receive an appreciable sympathetic influence from the SG. Like experimental studies, we also found an asymmetric response to unilateral SG block and a dominance, in most of our patients, of the left SG. The influence on myocardial refractoriness was less apparent.

The echocardiographic (echo) features of idiopathic hemochromatosis (IH) were studied in 22 patients. Results were compared with a control group of 22 patients without heart disease. Statistically significant increases in left ventricular (LV) mass, end-diastolic and end-systolic diameters of the left ventricle and in left atrial dimension were observed in patients with IH; significant changes of systolic function indexes (decrease in fractional shortening and ejection fraction and increase in distance of the E point to the septum) were seen as well. These echo abnormalities were mainly seen in patients with abnormal electrocardiograms. In 11 patients with IH, iron removal therapy was carried out by means of periodic phlebotomies. In patients with impaired LV function at the beginning of therapy, comparison between measurements of the initial echo and posttreatment echo showed significant improvement in LV diameters, fractional shortening, ejection fraction, distance from the E point to the septum, LV mass and left atrial dimension.

To analyze the behavior of aortic valve gradient (AVG) after ventricular extrasystole (VE), we studied 36 pure valvular aortic stenoses (AS) free of coronary artery disease and obstructive hypertrophic cardiomyopathy, in whom basal (B) (74 +/- 32 mm Hg) and catheter-induced post-VE (110 +/- 50 mm Hg) AVG were obtained. In all 26 cases with valve area less than 0.70 cm2, the post-VE AVG was greater than or equal to 70 mm Hg. In 19 cases AVG after two or more consecutive VE were also obtained. Maximal post-VE AVG was obtained after multiple VE (19 cases) and/or after one VE causing a post-VE pause equal or longer than 1.7 basal cardiac cycles (post-VE RR greater than or equal to 1.7 B RR) (9 cases). Basal and postsingle VE AVG, up to a post-VE RR greater than or equal to 1.7 B RR, were a linear function of previous RR (r greater than or equal to 0.90), regression line slope increasing with AS severity (P = .05). Inotropic state measured by PEP/LVET only increased after multiple VE, P less than .01. AVG after multiple VE was independent of post-VE RR. Thus, 1) post-VE potentiation of AVG may be seen with fixed valvular AS without obstructive cardiomyopathy; 2) post-VE AVG is a function of compensatory pause after single VE and of increased inotropism after multiple VE; 3) analysis of maximal post-VE AVG generated as described is reliable and useful for assessing AS severity (post-VE AVG greater than or equal to 70 mm Hg meaning an aortic valve area less than 0.70 cm2) and may supplement valve area calculations.

Seventy-eight consecutive episodes of infective endocarditis on native valves have been prospectively treated and followed-up after discharge from 1975 to 1982 (mean follow-up period 31 months). Twenty one patients needed valvular replacement in the active phase of the disease. Overall mortality was 15 cases, 7 from the medical group and 8 from the surgical group. At last clinical control 21 from the 46 survivors of the medical group remained asymptomatic, 17 had needed valvular replacement, 5 had died 2 of congestive heart failure and 3 (addicts) were lost to follow-up. From the 13 survivors of the surgical group 8 remained asymptomatic with good prosthetic function, 4 had needed reoperation due to severe periprosthetic leak and 1 died suddenly during follow-up. Figures at the end of follow-up showed that 28% of the initial patients had died, 39% carried a valvular prosthesis and 28% remained asymptomatic. A retrospective analysis of factors predictive of poor prognosis has been carried out.

Thirteen patients with tuberculous pericarditis (12 men and 1 woman aged 13 to 70 years [mean 41]) were identified in a group of 294 patients consecutively admitted for primary acute pericardial disease. The diagnosis was made by the following studies: sputum culture (n = 4), culture of pericardial fluid obtained by pericardiocentesis (n = 3), histologic study and culture of pericardial biopsy (n = 3), lymph node biopsy (n = 2) and plenral biopsy (n = 1). Clinical presentation was remarkably variable: four patients had an acute, apparently self-limited course, one had relapsing tamponade, four had tamponade effectively treated with pericardiocentesis and four had toxic symptoms with persistent fever. The interval from hospital admission to diagnosis ranged from 1 to 14 weeks (mean 5.2). Constrictive pericarditis developed in six patients and effusive-constrictive pericarditis in one; all seven required pericardiectomy 2 to 3.5 months after admission. No patient died.It is concluded that 1) tuberculous pericarditis has a variable clinical presentation and therefore it should be considered in the evaluation of all instances of pericarditis without a rapidly self-limited course; 2) the diagnosis should be based only on objective data obtained with a systematic study protocol; 3) early definitive diagnosis is still difficult to achieve; and 4) development of subacute constrictive pericarditis requiring pericardiectomy is common.

Twenty-nine consecutive spontaneous attacks of paroxysmal supraventricular tachycardia (PSVT) in 14 infants (mean age 4.4 months) were treated with verapamil. No infant had associated heart disease. Verapamil 1-2 mg i.v was administered over 30 seconds. The dosage varied according to the weight of the infant. Within 60 seconds sinus rhythm was obtained in 28 instances (96.5%). No significant complications were observed. The high effectiveness, rapid action and lack of undesirable side effects observed in this series suggest that verapamil is the drug of choice in the treatment of PSVT in infants without underlying heart disease.

To assess the usefulness of stress testing in predicting multivessel coronary disease and left ventricular dysfunction, 83 male patients with a myocardial infarction one to 84 months previously were studied. In inferior infarction (45 patients), the ST segment depression had a sensitivity of 91% and a specificity of 77% to detect multivessel disease. Patients with multivessel disease had significantly lower exercise capacity and maximal heart rates. ST segment elevation showed a poor correlation with the number of affected vessels. In anterior infarction (38 patients), both ST segment depression and elevation were of little value to detect multivessel disease. However, the predictive value of an exercise test without ST segment changes to exclude multivessel disease was 89%; on the other hand, patients without ST segment changes had significantly higher ejection fractions, exercise capacity, maximal heart rates and rate-pressure products than patients with ST segment changes. Patients with ST segment elevation had significantly lower ejection fractions in both groups. The sensitivity of ST segment elevation to detect severe segmental left ventricular dysfunction was 84% for anterior infarction and 54% for inferior infarction. Specificity was 84 and 85%, respectively. We conclude that: (1) exercise-induced ST segment depression is useful to predict the extent of coronary artery disease in inferior infarction, but it is of limited value in anterior infarction, (2) exercise-induced ST segment elevation correlates well with the presence of severe left ventricular dysfunction in both anterior and inferior infarction, and (3) an exercise test of considerable intensity without ST segment changes makes the existence of multivessel coronary disease and/or severe left ventricular dysfunction very improbable.

We prospectively studied 110 patients with a first acute myocardial infarction with cross–sectional echocardiography, between 7–10 days post–infarction, to assess the value of semiquantitative segmental con–tractility score for the first year post–AM I risk stratification. 87 patients had acceptable recordings (40 anterior and 47 inferior infarction). Twelve patients had severe complications (severe angina or heart failure, reinfarction or death) and 40 had nonsevere complications. The total segmental score was higher in complicated than in non–complicated patients. The score also differentiated angina from heart failure. The score of necrotic area was more discriminating than that of non-necrotic area. Discriminating power was higher in anterior than in inferior acute myocardial infarction. Thus we conclude that the semiquantitative assessment of segmental contractility by cross–sectional echocardiography is useful for risk stratification following acute infarction identifying severe complications, particularly heart failure, with better discrimination in anterior acute myocapdial infarction.

Incidence and significance of pericardial effusion in patients with acute myocardial infarction (AMI) have not been established. To evaluate these issues, we studied prospectively 138 consecutive patients with AMI. An echocardiogram was obtained in each 1, 3, and 10 days and 3 and 6 months after admission. Fifty four patients with unstable angina and 57 without heart disease were studied as controls. Echocardiographic diagnostic criteria of pericardial effusion were established from 33 additional patients undergoing surgery. Pericardial effusion was found in 28% of patients with AMI. Twenty-five percent of patients with AMI had pericardial effusion on the third day, vs 8% of patients with unstable angina (p less than .02) and 5% of patients without heart disease (p less than .01). At 1, 3, and 10 days and 3 and 6 months prevalence of pericardial effusion was 17%, 25%, 21%, 11%, and 8%, respectively. There was no case of tamponade. Pericardial effusion was more common in anterior AMI (p less than .02) and in patients with heart failure (p less than .05) but it was not significantly associated with early pericarditis, peak creatine kinase-MB, the level of anticoagulation, or mortality. Thus, pericardial effusion is a common event in patients with AMI (incidence of 28%), but does not result in specific complications. The reabsorption rate of pericardial effusion is slow and, in our experience, mild or moderate pericardial effusion does not preclude heparin therapy.

The echocardiographic findings of three patients with discrete subaortic stenosis associated with infective endocarditis are reported. This disorder was suspected because of early systolic aortic valve partial closure followed by a fine fluttering throughout systole in each case. Narrowing of the left ventricular outflow tract as judged by the left ventricular outflow tract/aortic root ratio was of limited diagnostic value because the presence of echoes of aortic vegetations at this level in two cases prevented accurate measurement of the outflow tract. This study suggests that a careful echocardiographic study may detect discrete subaortic stenosis in the presence of aortic valve endocarditis. Thus, whenever left ventricular outflow obstruction is associated with infective endocarditis, early systolic aortic valve partial closure followed by a fine fluttering throughout systole should be carefully sought

To investigate the usefulness of exercise-induced R wave changes in the diagnosis of coronary artery disease and detection of left ventricular contraction abnormalities, 105 patients were studied. Among 64 patients who had significant coronary artery disease (greater than or equal to 70% narrowing), 43 showed an increase or no change in the R wave amplitude and 55 showed ST segment depression (sensitivity 67 versus 86%). Among 41 patients without significant stenosis, 11 had decreased R wave amplitude and 36 had no change in ST segment (specificity 27 versus 88%). Twenty-five of 64 coronary disease patients had left ventricular contraction abnormalities, and the R wave amplitude changes gave a sensitivity of 80%, specificity of 41% and a predictive value of 47%. There were no differences in the variables of exercise intensity and ejection fraction between patients who had decreased R wave amplitude and those in whom it increased or did not change. We conclude that R wave amplitude change during exercise is not a useful variable for the diagnosis or evaluation of patients with coronary artery disease.

Objectives.Our aim was to use noninvasive studies early after infarction to assess medium-term prognosis in patients with a first uncomplicated myocardial infarction.Background.Although the use of early postinfarction assessment to gauge short-term prognosis in myocardial infarction is well established, there have been few comprehensive evaluations of noninvasive methods for assessing medium- and long-term prognosis.Methods.We prospectively studied 115 consecutive patients

Objectives. This study sought to evaluate the effects of prolonged rest and blood pressure control on survival of patients in whom left ventricular free wall rupture (LVFWR) was strongly suspected. Background. Left ventricular free wall rupture in myocardial infarction is often fatal, and only a few patients may undergo operation. However, survival without surgical repair has not yet been evaluated. Methods. Eighty-one consecutive patients with a first transmural acute myocardial infarction in Killip class I or II who presented with acute hypotension due to cardiac tamponade, with electromechanical dissociation (EMD) in 72, were prospectively evaluated. Patients with early recovery were managed with prolonged bed rest and blood pressure control with beta-blockade as tolerated. Results. Forty-seven patients died within 2 h of acute tamponade, and autopsy in 21 showed LVFWR in all. In 15 others, an emergency surgical repair resulted in 2 survivors. The remaining 19 patients, 10 with EMD, had early recovery with dobutamine and colloid solution, and 15 required pericardiocentesis. Shortly thereafter, these 19 patients still showed a paradoxic pulse ≥20 mm Hg, relevant pericardial effusion (24 ± 7 mm [mean ± SD]) and comparable elevation of right and left ventricular filling pressures (15.8 ± 3.9 and 15.9 ± 3.8 mm Hg, respectively). Subsequent management included bed rest (8.2 ± 4.8 days) and control of systolic blood pressure (≤120 mm Hg) with beta-adrenergic blocking agents as tolerated (n = 12). Four patients died, and autopsy in three revealed a rupture that was sealed in two. A sealed rupture was also seen at thoracotomy in 2 other patients who, like the remaining 13, survived for 52.5 ± 35.2 months. Conclusions. Long-term survival of selected patients with prompt hemodynamic recovery after LVFWR is possible without surgical repair. Prolonged bed rest and blood pressure control are likely to contribute favorably to their initial outcome. (J Am Coll Cardiol 1997;29:512–8)

Objectives.We attempted to ascertain whether cardiac index can be directly estimated from Doppler mean velocity.Background.Although diverse Doppler echocardiographic methods have been described for cardiac output quantification, they are not widely used in clinical practice. Cross-sectional area measurement has been identified as the main source of error in flow volume quantification.Methods.A three-phase study by Doppler echocardiography was conducted in 306 patients. In phase I, the normal mean velocity ratio of the left and right ventricular outflow tracts was established in 170 normal subjects. In phase II, cardiac index, calculated as the product of aortic annular area index by mean velocity (conventional method), and mean velocity determined in the left ventricular outflow tract and ascending aorta by pulsed and continuous wave Doppler, respectively, were correlated with thermodilution cardiac index in 66 patients. In phase III, the accuracy of the regression equations obtained was prospectively assessed in an additional 70 patients.Results.The normal left/right ventricular outflow tract mean velocity ratio by pulsed wave Doppler was 1.1 ± 0.1. Cardiac index (CI) calculated by the conventional method and thermodilution (TD) showed acceptable correlation (r = 0.90, CITD= 1.20 CIPWD+ 357; r = 0.86, CITD= 0.90 CICWD+ 262) for pulsed (PWD) and continuous wave (CWD) Doppler, respectively, but with systematic underestimation (−28 ± 13%, p < 0.01) by pulsed wave Doppler. Mean velocity (MV) showed excellent correlation with the thermodilution cardiac index (r = 0.97, CITD= 172 MVPWD−172; r = 0.93, CITD= 129 MVCWD−255). When these regression equations were prospectively applied, better agreement with the thermodilution cardiac index was obtained by pulsed wave Doppler directly from mean velocity (SD 240 ml/min per m2) than when aortic annular area was considered in the calculation (SD 428 ml/min per m2). Similar results were obtained by continuous wave Doppler (SD 433 vs. 599 ml/min per m2) but with less accuracy.Conclusions.Left ventricular outflow tract mean velocity determined by pulsed wave Doppler permits easy, accurate cardiac index quantification in the absence of left ventricular outflow abnormalities. The simplicity of this method enhances its clinical applicability in noninvasive monitoring of cardiac index.

Objective : The hypothesis was that Na + /H + exchange occurring during normothermic cardioplegia contributes to the development of myocardial edema during subsequent reperfusion and impairs functional recovery. Methods : Rat hearts were perfused in a Langendorff apparatus and submitted to 60 minutes of normothermic cardioplegia and 90 minutes of reperfusion. Hearts were allocated to one of four groups ( n = 8): inhibition of Na + /H + exchanger with HOE642 throughout the whole experiment (HOE group), only during cardioplegia (HOE-C) or during reperfusion (HOE-R), and a control group. Results : In HOE and HOE-C groups, myocardial water content at the end of reperfusion was lower than in the HOE-R and control groups (526 ± 19 and 533 ± 18 ml/100 gm dry tissue vs 632 ± 25 and 634 ± 17 ml/100 gm dry tissue, respectively, p = 0.001), left ventricular end-diastolic pressure increased less after reperfusion (46.6 ± 9.7 and 63.2 ± 10.0 mm Hg vs 75.1 ± 4.3 mm Hg and 85.7 ± 8.9 mm Hg, respectively, p = 0.006), and recovery of left ventricular developed pressure was better (46.7% and 45.8% vs 4.5% and 9.8%, p = 0.048). Relative to the control group, total lactate dehydrogenase release during reperfusion was reduced by 80.2%, 69.3% and 36% in HOE, HOE-C, and HOE-R groups, respectively. Conclusion : Inhibition of the Na + /H + exchange during normothermic cardioplegia reduces myocardial edema and necrosis during subsequent reperfusion, improving functional recovery. Inhibition of Na + /H + exchange during reperfusion only has a much smaller effect. (J Thorac Cardiovasc Surg 1998;115:709-15)

A case of a transient and huge postanterior acute myocardial infarction left ventricular thrombus causing temporary intractability of severe heart failure is reported. Echo-graphic and hemodynamic data suggest the restrictive-obliterative pattern of heart failure.

improve the outcome of endomyocardial fi brosis;' therefore, any finding helping to distinguish this condition from other cardiac diseases will be of unquestionable interest. Few reports of echocardio graphic findings in endomyocardial fibrosis are available.'3 We report a patient with autopsy proved endomyocardial fibrosis whose echocardio gram showed striking features allowing suggestion of the correct diagnosis.

Two patients who had a huge pericardial effusion of at least 9 and 14 years' duration caused by cardiac toxoplasmosis are reported. Toxoplasma gondii were seen in the pericardial fluid, and serologic evidence also demonstrated the activity of the infection. These cases illustrate both the need to exclude toxoplasmosis in chronic pericardial effusion of unknown cause and the possibility of seeing toxoplasma in the pericardial fluid of patients with active toxoplasmic pericarditis. Moreover, in endemic areas, cardiac toxoplasmosis may not be an exceptional cause of chronic pericardial effusion.

Forty-nine consecutive patients (44 with atrial fibrillation and five with atrial flutter) received 10 mg of verapamil five to seven minutes before elective electroversion, to evaluate the feasibility of the latter while verapamil effects were present. Excluded were patients with moderate-to-severe heart failure, acute myocardial infarction, mean ventricular rate lower than 70 beats/minute, those receiving any antiarrhythmic drug other than digoxin, and those in whom sinus node dysfunction was suspected. In six patients, eight complications took place: four instances of hypotension (systolic blood pressure below 80 mm Hg), two instances of junctional escape rhythm (47 and 63 beats/minute) and two instances of junctional tachycardia. In all four instances of hypotension, return to normal values of blood pressure was spontaneous (within five minutes in three patients). Rhythm disturbances were transient, without clinical relevance. This study suggests that electroversion can be safely carried out during clinical action of verapamil in properly selected patients, and that occasional, self-limited hypotension is the only complication of clinical significance to be expected.

Mitral area is the parameter used for quantitating mitral stenosis (MS) severity. When mitral gradient (MG) is low and reduction of mitral valve area (MVA) might be critical, interventions presumably increasing mitral valve flow (MVF), such as stress or atrial pacing, have been carried out. The purpose of this study was to analyze in 28 patients the combined effect of left ventriculography (LVG) and intravenous atropine (ATR) in the hemodynamic evaluation of MS. The rationale for combining these two interventions is to add up the ATR-positive chronotropic effect to the LVG potentiation of cardiac output. The LVG plus ATR markedly accelerated heart rate (from 80 +/- 14 to 104 +/- 18 bts/min, P less than 0.001), mildly increased cardiac index (from 2.6 +/- 0.6 to 2.9 +/- 0.6 1/min/m2, P less than 0.05), and importantly increased MVF (from 136 +/- 30 to 172 +/- 46 ml/bt, P less than 0.001). Pulmonary wedge pressure increased (from 14 +/- 5 to 21 +/- 5 mmHg, P less than 0.001) because of an important increment of MG (from 12 +/- 6 to 18 +/- 7 mmHg, P less than 0.001). None of six cases with mild MS (MVA greater than 1.5 cm2) and nine of ten cases with severe MS (MVA less than or equal to 1.0 cm2) had MG after LVG plus ATR greater than 12 mmHg. The remaining case with severe MS and the two cases (out of 12) with moderate MS having MG after LVG plus ATR less than or equal to 12 mmHg had, at surgical evaluation, noncritically reduced MVA. This study shows that LVG plus ATR is a valid and easy intervention for increasing MVF during cardiac catheterization. It also allows the reclassification of patients with low baseline MG and reduced MVA into two subgroups: Cases with critically reduced MVA at surgery achieve a postintervention MG greater than 12 mmHg and those cases with noncritically reduced MVA achieve a postintervention MG less than or equal to 12 mmHg.

The dynamic behavior of fixed LV outflow tract stenosis partly resembles that of OCM. To analyze their differences we studied basal and postextrasystolic (post-PVC) peak-to-peak LV aortic gradients, aortic systolic pressure, and pulse pressure in 14 OCM and in 36 pure VAS without two-dimensional echocardiographic findings of OCM. Fifteen mild VAS had basal gradients similar to those of OCM (39 +/- 17 mm Hg vs 24 +/- 16 mm Hg). Patients with OCM show a post-PVC gradient (109 +/- 41 mm Hg) similar to that of VAS (110 +/- 50 mm Hg). However, the latter were departing from much higher gradients (VAS 72 +/- 30 mm Hg vs OCM 24 +/- 16 mm Hg). Decrement of post-PVC aortic systolic pressure and pulse pressure were frequent in both groups, but decrement of pulse pressure greater than 5 mm Hg were more frequent in OCM. We concluded that (1) post-PVC increased aortic gradients and decreased aortic systolic pressure occurred in both VAS and OCM; (2) post-PVC decreased aortic pulse pressure might occur in VAS; and (3) association of post-PVC gradient increment greater than 75 percent and pulse pressure decrement greater than 5 mm Hg are strongly suggestive of OCM.

Since the introduction by Gorlin and Gorlin of the hydraulic formulae for calculating valve area, it has become the best parameter for quantitating valve stenosis. Recently Hakki et al proposed a simplified formula for valve area calculation that does not take into account either heart rate (HR) or left ventricular filling or ejection time. The purpose of this study was to analyze the validity of Hakki's formulae under different physiological conditions and to propose an easy correction to improve its accuracy. Our study suggests: (1) that an easy correction for heart rate in certain cases, dividing by 1.35 when HR less than 75 beats per min in mitral stenosis and when HR greater than 90 beats per min in aortic stenosis, significantly improves the accuracy and validity of Hakki's formulae (p less than 0.02 and p less than 0.05); (2) the instantaneous valve gradients (peak gradient for aortic stenosis and average of instantaneous early, middle, and late diastolic gradients for mitral stenosis) are as valid as mean planimetric gradients for valve area calculation. Thus the simplified formulae proposed in this study allow mitral and aortic valve area calculations by means of instantaneous gradients, cardiac output, and heart rate.