Patricia C. Come

Left ventricular remodeling after myocardial infarction: a corollary to infarct expansion.

Dilatation of infarcted segments (infarct expansion) may occur during recovery from myocardial infarction, but the fate of noninfarcted segments is uncertain. Accordingly, left ventricular geometric changes were assessed by left ventricular angiography and M mode echocardiography on admission and 2 weeks later in 30 patients with their first acute transmural myocardial infarction. All patients demonstrated chest pain, ST segment elevation with subsequent development of Q waves (15 anterior, 15 inferior), and elevation of cardiac enzymes. Sequential left ventricular angiographic and hemodynamic findings were available in these patients by virtue of their participation in a study of thrombolysis in acute myocardial infarction. By that study design, all patients treated successfully with thrombolytic therapy and demonstrating improvement of flow in an occluded coronary artery underwent repeat cardiac catheterization. At 2 weeks there was a significant decrease in left ventricular and pulmonary capillary wedge pressures (p less than .01), whereas both left ventricular end-diastolic (LVEDV) and end-systolic (LVESV) volume indexes increased (p less than .01). The increase in LVEDV correlated directly with the percentage of the ventriculographic silhouette that was akinetic or dyskinetic at the initial catheterization (r = .71, p less than .001). To assess regional changes in both infarcted and noninfarcted segments, serial endocardial perimeter lengths of both the akinetic-dyskinetic segments (infarction zone) and of the remainder of the cardiac silhouette (noninfarction zone) were measured in all patients who demonstrated at least a 20% increase in their LVEDV at 2 weeks after myocardial infarction. Notably, there was a mean increase of 13% in the endocardial perimeter length of infarcted segments and a 19% increase in the endocardial perimeter length of noninfarcted segments. Serial M mode echocardiographic studies showed no significant change in the wall thickness of noninfarcted myocardial segments. Hemodynamic changes that occurred in this subgroup of patients included significant decreases in left ventricular end-diastolic and pulmonary capillary wedge pressures (p less than .05) and significant increases in angiographic cardiac index (p less than .01) and LVESV index (p less than .01). We conclude that in patients who manifest cardiac dilatation in the early convalescent period after myocardial infarction, there is remodeling of the entire left ventricle including infarct expansion of akinetic-dyskinetic segments and volume-overload hypertrophy of noninfarcted segments.(ABSTRACT TRUNCATED AT 400 WORDS)

Alteplase versus heparin in acute pulmonary embolism: randomised trial assessing right-ventricular function and pulmonary perfusion

Data from a non-randomised study have hinted that in patients with acute pulmonary embolism (PE), thrombolysis followed by heparin more rapidly reverses right-ventricular dysfunction and restores pulmonary tissue perfusion than does heparin alone. We have pursued this idea in a randomised protocol. 46 haemodynamically stable patients were randomised to recombinant tissue plasminogen activator (alteplase, rt-PA) 100 mg over 2 h followed by intravenous heparin and 55 to heparin alone. Right-ventricular wall motion was assessed qualitatively, and right-ventricular end diastolic area was estimated by planimetry from echocardiograms at baseline and at 3 and 24 hours. Pulmonary perfusion scans were obtained at baseline and 24 hours. In 39% of rt-PA patients but in only 17% of heparin alone patients right-ventricular wall motion at 24 hours had improved from baseline and in 2% and 17%, respectively, it worsened (p = 0.005). rt-PA patients also had a significant decrease in right-ventricular end-diastolic area during the 24 hours after randomisation and a significant absolute improvement in pulmonary perfusion (14.6% vs 1.5%). No clinical episodes of recurrent PE were noted among rt-PA patients, but there were 2 fatal and 3 non-fatal clinically suspected recurrent PEs within 14 days in patients randomised to heparin alone. rt-PA rapidly improves right-ventricular function and pulmonary perfusion among patients with PE and may lead to a lower rate of adverse clinical outcomes.

Balloon aortic valvuloplasty in 170 consecutive patients

Between October 1, 1985, and April 1, 1988, we performed balloon aortic valvuloplasty in 170 patients (mean age [+/- SD], 77 +/- 5 years) who had symptomatic aortic stenosis. The procedure was completed successfully in 168 patients and resulted in significant increases in the mean (+/- SD) aortic-valve area (from 0.6 +/- 0.2 to 0.9 +/- 0.3 cm2) and cardiac output (from 4.6 +/- 3.4 to 4.8 +/- 1.4 liters per minute) and decreases in the peak aortic-valve pressure gradient (from 71 +/- 20 to 36 +/- 14 mm Hg) (P less than 0.01 for all three comparisons). There were six in-hospital deaths, and five patients required early aortic-valve replacement. Follow-up data were available for all patients, for a period averaging 9.1 months. In addition to the 6 patients who died in the hospital, 25 patients died an average of 6.4 +/- 5.3 months after discharge. Symptoms recurred in 44 patients; they were managed by repeat valvuloplasty in 16 patients, by aortic-valve replacement in 17, and by medical therapy in 11. At the most recent follow-up examination, the symptoms of 103 patients had improved after valvuloplasty; this number includes 15 patients with restenosis who successfully underwent redilation. Life-table analysis indicates that the probability of survival 12 months after the procedure was 74 percent. We conclude that balloon aortic valvuloplasty is an effective palliative therapy for some elderly patients with symptomatic aortic stenosis. Symptoms improve in the majority of patients; although restenosis is common, it can be managed in some patients by repeat balloon dilation.

Balloon dilation of mitral stenosis in adult patients: postmortem and percutaneous mitral valvuloplasty studies.

Preliminary reports have documented the utility of percutaneous balloon valvuloplasty of the mitral valve in adult patients with mitral stenosis, but the mechanism of successful valve dilation and the effect of mitral valvuloplasty on cardiac performance have not been studied in detail. Accordingly, mitral valvuloplasty was performed in five postmortem specimens and in 18 adult patients with rheumatic mitral stenosis, using either one (25 mm) or two (18 and 20 mm) dilation balloons. Postmortem balloon dilation resulted in increased valve orifice area in all five postmortem specimens, secondary to separation of fused commissures and fracture of nodular calcium within the mitral leaflets. In no case did balloon dilation result in tearing of valve leaflets, disruption of the mitral ring or liberation of potentially embolic debris. Percutaneous mitral valvuloplasty in 18 patients with severe mitral stenosis (including 9 with a heavily calcified valve) resulted in an increase in cardiac output (4.3 +/- 1.1 to 5.1 +/- 1.5 liters/min, p less than 0.01) and mitral valve area (0.9 +/- 0.2 to 1.6 +/- 0.4 cm2, p less than 0.0001), and a decrease in mean mitral pressure gradient (15 +/- 5 to 9 +/- 4 mm Hg, p less than 0.0001), pulmonary capillary wedge pressure (23 +/- 7 to 18 +/- 7 mm Hg, p less than 0.0001) and mean pulmonary artery pressure (36 +/- 12 to 33 +/- 12 mm Hg, p less than 0.01). Left ventriculography before and after valvuloplasty in 14 of the 18 patients showed a mild (less than or equal to 1+) increase in mitral regurgitation in five patients and no change in the remainder.(ABSTRACT TRUNCATED AT 250 WORDS)

Nitroglycerin-induced severe hypotension and bradycardia in patients with acute myocardial infarction.

SUMMARY Seven episodes of simultaneous severe systemic arterial hypotension and absolute or relative bradycardia were observed in five patients receiving either sublingual nitroglycerin (two patients) or intravenous nitroglycerin (three patients) within the first 24 hours of onset of symptoms of acute myocardial infarction. Left ventricular filling pressure, measured as pulmonary artery diastolic pressure, decreased simultaneously in all four patients in whom pulmonary artery pressures were monitored. No initial increase in heart rate was observed in any of the five patients prior to the development of bradycardia. Possible mechanisms producing simultaneous bradycardia and hypotension during nitroglycerin administration are considered. The patient studies emphasize the importance of careful hemodynamic monitoring during administration of sublingual or intravenous nitroglycerin to patients with acute myocardial infarction.

Prognostic significance of right ventricular hypokinesis and perfusion lung scan defects in pulmonary embolism

We studied the relation between right ventricular (RV) hypokinesis on echocardiography and defects on the initial perfusion lung scan among 90 hemodynamically stable patients with pulmonary embolism (PE). Of the 90, 38 had qualitative evidence of RV hypokinesis, with a mean RV end-diastolic area significantly larger than those with normal RV wall motion (40.0 +/- 10.2 cm2 vs 20.1 +/- 6.4 cm2; p < 0.001). The degree of the perfusion defect was greater in those patients with baseline RV hypokinesis (54% +/- 16% of the lung nonperfused) than in those patients with normal RV wall motion at baseline (30% +/- 18% nonperfused lung; p < 0.001). Receiver operating characteristic curve analysis showed that a perfusion lung scan defect score of 0.3 (i.e., 30% of the lung nonperfused) had a 92% sensitivity for predicting RV hypokinesis and carried a relative risk for observing RV hypokinesis of 6.8 times greater than among those patients with a perfusion scan score of < 0.3. Considering that all patients with recurrent symptomatic PE were in the subgroup with RV hypokinesis (13% vs 0% for those with normal RV wall motion; p = 0.01), a strategy of performing echocardiography in those patients with a perfusion scan defect score of > or = 0.3 appears to identify patients at increased risk for recurrent PE.

Early reversal of right ventricular dysfunction in patients with acute pulmonary embolism after treatment with intravenous tissue plasminogen activator

To assess abnormalities of right heart function and their reversal with thrombolysis in pulmonary embolism, serial imaging and Doppler echocardiographic studies were performed before and after a 6 hour intravenous infusion of 80 to 90 mg of recombinant tissue-type plasminogen activator (rt-PA) in seven patients with segmental or lobar acute pulmonary embolism. None of the five men and two women had known prior pulmonary hypertension. Substantial clot lysis and improvement in pulmonary blood flow, as determined by serial pulmonary angiography and perfusion lung scanning, were achieved in all. Coincident with clot lysis, pulmonary artery systolic pressure decreased (from 42 +/- 11 to 26 +/- 7 mm Hg, p less than 0.005), right ventricular diameter decreased (from 3.9 +/- 1.0 to 2.0 +/- 0.5 cm, p less than 0.005) and left ventricular diameter increased (from 3.7 +/- 0.9 to 4.4 +/- 0.6 cm, p less than 0.01). Right ventricular wall movement, initially mildly, moderately or severely hypokinetic in one, two and four patients, respectively, normalized in five and improved to mild hypokinesia in two. Tricuspid regurgitation was present before lytic therapy in six patients. In five, flow velocity in the tricuspid regurgitant jets indicated a peak systolic right ventricular minus right atrial pressure gradient of 25 to 52 mm Hg. Tricuspid regurgitation was detected early after lytic therapy in only two patients. Systolic septal flattening was noted before but not after lysis. These findings confirm that pulmonary emboli may result in appreciable right ventricular dysfunction and dilation, resultant tricuspid regurgitation, abnormal septal position and decreased left ventricular size.(ABSTRACT TRUNCATED AT 250 WORDS)

Assessment of left ventricular and aortic valve function after aortic balloon valvuloplasty in adult patients with critical aortic stenosis.

Preliminary reports have documented the utility of balloon aortic valvuloplasty as a palliative treatment for high-risk patients with critical aortic stenosis, but the effect of this procedure on cardiac performance has not been studied in detail. Accordingly, 32 patients (mean age 79 years) with long-standing, calcific aortic stenosis were treated at the time of cardiac catheterization with balloon dilatation of the aortic valve, and serial changes in left ventricular and valvular function were followed before and after valvuloplasty by radionuclide ventriculography, determination of systolic time intervals, and Doppler echocardiography. Prevalvuloplasty examination revealed heavily calcified aortic valves in all patients, a mean peak-to-peak aortic valve gradient of 77 +/- 27 mm Hg, a mean Fick cardiac output of 4.6 +/- 1.4 liters/min, and a mean calculated aortic valve area of 0.6 +/- 0.2 cm2. Subsequent balloon dilatation with 12 to 23 mm valvuloplasty balloons resulted in a fall in aortic valve gradient to 39 +/- 15 mm Hg, an increase in cardiac output to 5.2 +/- 1.8 liters/min, and an increase in calculated aortic valve area to 0.9 +/- 0.3 cm2. Individual hemodynamic responses varied considerably, with some patients showing major increases in valve area, while others demonstrated only small increases. In no case was balloon dilatation accompanied by evidence of embolic phenomena. Supravalvular aortography obtained in 13 patients demonstrated no or a mild (less than or equal to 1+) increase in aortic insufficiency. Serial radionuclide ventriculography in patients with a depressed left ventricular ejection fraction (i.e., that less than or equal to 55%) revealed a small increase in ejection fraction from 40 +/- 13% to 46 +/- 12% (p less than .03). In addition, for the study group as a whole there was a decrease in left ventricular end-diastolic volume index (113 +/- 38 to 101 +/- 37 ml/m2, p less than .003), a fall in stroke-volume ratio (1.49 +/- 0.44 to 1.35 +/- 0.33, p less than .04), and no immediate change in left ventricular peak filling rate (2.05 +/- 0.77 to 2.21 +/- 0.65 end-diastolic counts/sec, p = NS). Serial M mode echocardiography and phonocardiography showed an increase in aortic valve excursion (0.5 +/- 0.2 to 0.8 +/- 0.2 cm, p less than .001), a decrease in time to one-half carotid upstroke (80 +/- 30 to 60 +/- 10 msec, p less than .001), and a small decrease in left ventricular ejection time (0.44 +/- 0.03 to 0.42 +/- 0.02 sec, p less than .001).(ABSTRACT TRUNCATED AT 400 WORDS)

Reversal by Phenylephrine of the Beneficial Effects of Intravenous Nitroglycerin in Patients with Acute Myocardial Infarction

Nitroglycerin has been shown to reduce ST-segment elevation during acute myocardial infarction, an effect potentiated in the dog by agents that reverse nitroglycerin-induced hypotension. Our study was designed to determine the effects of combined nitroglycerin and phenylephrine therapy. Ten patients with acute transmural myocardial infarctions received intravenous nitroglycerin, sufficient to reduce mean arterial pressure from 107 +/- 6 to 85 +/- 6 mm Hg (P less than 0.001), for 60 minutes. Left ventricular filling pressure decreased from 19 +/- 2 to 11 +/- 2 mm Hg (P less than 0.001). SigmaST, the sum of ST-segment elevations in 16 precordial leads, decreased (P less than 0.02) with intravenous nitroglycerin. Subsequent addition of phenylephrine infusion, sufficient to re-elevate mean arterial pressure to 106 +/- 4 mm Hg (P less than 0.001) for 30 minutes, increased left ventricular filling pressure to 17 +/- 2 mm Hg (P less than 0.05) and also significantly increased sigmaST (P less than 0.05). Our results suggest that addition of phenylephrine to nitroglycerin is not beneficial in the treatment of patients with acute myocardial infarction.

Effects of intravenous nitroglycerin on left ventricular function and ST segment changes in acute myocardial infarction.

It has been shown previously that 30-minute infusions of intravenous nitroglycerin in patients with acute myocardial infarction are able to lower left ventricular filling pressure and improve left ventricular function while lowering mean arterial pressure by only 7 mmHg (0.9 kPa). A decrease in sigmaST in praecordial ST segment mapping studies during nitroglycerin infusion in patients with anterior infarction suggested a decrease in the extent of myocardial ischaemia. In the present study, 30 patients with acute myocardial infarction received 1- to 3-hour infusions of intravenous nitroglycerin at infusion rates sufficient to lower mean arterial pressure by an average of 22 mmHg (2.9 kPa). An improvement in ventricular function was noted in that subgroup of patients with the msot severe left ventricular dysfunction. All patients with anterior myocardial infarction underwent serial ST segment mapping and, irrespective of the presence or absence of left ventricular failure, showed a decrease in sigmaST during nitroglycerin infusion (P less than 0.005). These findings suggest that infusion of nitroglycerin improves left ventricular function and/or alters left ventricular compliance in patients with left ventricular failure complicating myocardial infarction and furthermore decreases sigmaST in all patients, irrespective of the presence or absence of left ventricular failure, suggesting that the extent of myocardial ischaemia is decreased.