Julian M. Aroesty

Simultaneous assessment of left ventricular systolic and diastolic dysfunction during pacing-induced ischemia.

Both systolic and diastolic dysfunction have been described during pacing-induced ischemia, but the temporal sequence of systolic and diastolic impairment has not been established. Accordingly, 22 patients with coronary artery disease were paced at increasing heart rates and studied with simultaneous hemodynamic monitoring, electrocardiographic recording, and radionuclide ventriculography. In addition, with synchronized left ventricular pressure tracings and radionuclide volume curves, three sequential pressure-volume diagrams were constructed for each patient corresponding to baseline, intermediate, and maximum pacing levels. Eleven patients (group I) demonstrated a nonischemic response to pacing tachycardia without chest pain, significant electrocardiographic changes, or significant rise in left ventricular end-diastolic pressure (LVEDP) in the immediate postpacing period. These patients demonstrated a progressive decrease in LVEDP, end-diastolic volume, and end-systolic volume, no change in cardiac output or left ventricular ejection fraction, and a progressive increase in left ventricular diastolic peak filling rate and the end-systolic pressure-volume ratio. Pressure-volume diagrams shifted progressively leftward and slightly downward, suggesting both an increase in contractility and a mild increase in left ventricular distensibility. The remaining 11 patients (group II) exhibited an ischemic response to pacing tachycardia, with each patient experiencing angina pectoris, demonstrating greater than 1 mm ST segment depression on the electrocardiogram, and exhibiting greater than 5 mm Hg rise in LVEDP immediately after pacing. LVEDP, end-diastolic volume, and end-systolic volume in these patients initially decreased and then subsequently increased during angina, with no change in cardiac output but a decrease in ejection fraction. Left ventricular peak diastolic filling rate and the left ventricular end-systolic pressure-volume ratio both increased at the intermediate pacing rate but fell at maximum pacing. Pressure-volume diagrams for these patients shifted leftward initially, then back to the right, during intermediate and peak pacing levels, often with an upward shift in the diastolic pressure-volume relationship. LVEDP in group II was significantly higher than that in group I at the intermediate pacing level with no difference in end-diastolic or end-systolic volumes, suggesting decreased left ventricular distensibility in these patients before the onset of systolic dysfunction at the maximum pacing level.(ABSTRACT TRUNCATED AT 400 WORDS)

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)

Percutaneous mitral valvuloplasty in an adult patient with calcitic rheumatic mitral stenosis

A 75 year old man with long-standing rheumatic mitral stenosis who refused surgical intervention was treated with percutaneous balloon valvuloplasty. Prevalvuloplasty evaluation revealed a heavily calcified mitral valve, a mean transvalvular gradient of 18 mm Hg, a Fick cardiac index of 1.7 liters/min per m2, a mitral valve area of 0.6 cm2 and 1 + mitral regurgitation. After transeptal catheterization and balloon dilation of the interatrial septum with an 8 mm angioplasty balloon, a 25 mm valvuloplasty balloon was advanced over a guide wire across the interatrial septum and positioned across the mitral anulus. Subsequent balloon inflation at 3 atm pressure resulted in a reduction of the mean mitral valve gradient to 12 mm Hg, an increase in cardiac index to 2.5 liters/min per m2, an increase in mitral valve area in 1.4 cm2 and an increase in mitral regurgitation from 1 + to 2 +. Valvuloplasty was well tolerated without embolization of clot or valvular debris, and resulted in marked clinical improvement with decreased dyspnea and increased exercise tolerance. Repeat catheterization 2 months after valvuloplasty showed further resolution of pulmonary hypertension and no evidence of valvular restenosis or worsening mitral regurgitation, but detected a small atrial septal defect with a pulmonary to systemic blood flow ratio of 1.8. It is concluded that percutaneous valvuloplasty is possible in the adult patient with calcific rheumatic mitral stenosis, and may result in a significant improvement in valvular function without producing life-threatening complications.

Assessment of the end-systolic pressure-volume relationship in human beings with the use of a time-varying elastance model.

The analysis of left ventricular end-systolic pressure-volume relationships in human beings has been hindered by the lack of a practical method of serial volume assessment and by an imprecise definition of end-systole. Modifications of the end-systolic relationship that have been used to circumvent these problems have included the use of single-point end-systolic pressure-volume ratios, the use of peak systolic pressure/minimum ventricular volume points for end-systolic points, and the use of end-ejection as a marker for end-systole. To assess the correlation between the parameters generated by these modifications with the slope (Emax) and volume intercept (VO) of the end-systolic line as defined by Sagawas model of time-varying elastance, simultaneous measurement of left ventricular pressure and gated radionuclide volume was made in 26 patients under various loading conditions and pressure-volume diagrams were constructed for each loading condition from 32 simultaneous pressure-volume coordinates. Two pressure-volume diagrams were recorded in 14 patients and three pressure-volume diagrams were recorded in 12 patients. Emax and VO were determined in all patients from the slope and volume intercept of the isochronic pressure-volume line with the maximum time-varying elastance as described by Sagawas model and were designated true Emax and true VO, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Evaluation of the association of proximal coronary culprit artery lesion location with clinical outcomes in acute myocardial infarction

Impaired coronary artery blood flow and left anterior descending (LAD) artery culprit location are angiographic variables that have been associated with poorer outcomes after fibrinolytic administration in patients with acute myocardial infarction (AMI). We hypothesized that culprit lesion location in the proximal portion of the culprit artery would also be associated with poorer clinical outcomes compared with a mid or distal location. Lesion location and clinical outcomes were evaluated in 2,488 patients from the Thrombolysis In Myocardial Infarction (TIMI) 4, 10A, 10B, and 14 trials. Proximal lesions were located before or at the first major branch of the parent artery, mid lesions were between the first and the second major branches, and all other lesions were classified as distal. Proximal lesions were associated with a higher incidence of in-hospital death or recurrent AMI compared with mid or distal lesions (10.5% [n = 478] vs 6.1% [n = 1,498] vs 3.7% [n = 511], p <0.001), and they were associated with a higher rate of in-hospital death (6.7% [n = 478] vs 3.2% [n = 1,498] vs 2.5% [n = 511], p = 0.001). In a multiple logistic regression model adjusting for TIMI flow grade, age, gender, and pulse, the planimetered distance from the ostium to the LAD culprit lesion was associated with 30-day death or recurrent AMI (odds ratio 0.79 per centimeter increase in distance down the artery, p = 0.01). Proximal culprit lesion location is associated with an increased risk of adverse outcomes after fibrinolytic administration, which is likely due to a larger area of subtended myocardium. In patients with a LAD culprit lesion, proximal lesion location is a multivariate correlate of adverse outcomes even after adjustment for coronary blood flow and other covariates.

Usefulness of percutaneous transluminal coronary angioplasty for unstable angina pectoris after non-Q-wave acute myocardial infarction

Without revascularization, patients with non-Q-wave acute myocardial infarction (AMI) are predisposed to angina, recurrent AMI and cardiac death. Percutaneous transluminal coronary angioplasty (PTCA) was performed in 68 patients with angina an average of 2.3 months after non-Q-wave AMI (41 anterior, 27 inferior). Mean diameter stenosis was 95%, with collateralized total occlusion of the infarct-related artery in 23 patients. PTCA was successful in 87% (59 of 68), with a mean residual stenosis of 30%. One patient had emergency bypass surgery. Long-term follow-up (average 17 +/- 10 months) was available for 58 of the 59 patients in whom PTCA was successful. Recurrent angina developed in 41% (24 of 58), but was relieved by repeat PTCA in 14, by late coronary artery bypass surgery in 4 and by medical therapy in 6. There was 1 nonfatal AMI, due to progressive disease in a nondilated vessel, and 1 noncardiac death At last follow-up, 46 of 58 patients (79%) were asymptomatic and fully active or employed. Thus, patients undergoing PTCA for angina after non-Q-wave AMI appear to have a relatively high clinical restenosis rate, but with repeat PTCA have a low incidence of subsequent angina, AMI and cardiac death.

Role of the Coronary Collateral Circulation in the Preservation of Left Ventricular Function

An angiographic assessment of the coronary arteries, the presence and quality of arterial collateralization and segmental left ventricular (LV) wall motion indicated that (a) in the presence of total or subtotal obstruction of a coronary artery, there was a significantly higher incidence of normal motion (p less than 0.001) if the segment of LV wall was supplied by good rather than poor collaterals, and (b) normal wall motion with good arterial collateralization was not associated with abnormal Q waves. It is concluded that a positive correlation exists between the quality of collateral filling and the preservation of LV wall motion in the area supplied.

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.

Medically refractory unstable angina pectoris. I. Long-term follow-up of patients undergoing intraaortic balloon counterpulsation and operation.

Of 82 patients with medically refractory unstable angina pectoris seen between October 1972 and January 1978, 60 patients underwent a combination of intraaortic balloon pump counterpulsation, cardiac catheterization and coronary revascularization. Most patients had atherosclerotic involvement of the vessels of the anterior left ventricular wall, 48 patients (80 percent) had abnormalities of left ventricular wall contraction and 22 patients (36 percent) had evidence of acute myocardial injury. One operative and one late death occurred. The perioperative infarction rate was 5 percent. Survivors, followed up for 3 to 63 months (mean 31 months), have done remarkably well; 77 percent are considered employable,and more than 90 percent are in functional class I or II.

Ischemia Detected on Continuous Electrocardiography After Acute Coronary Syndrome: Observations From the MERLIN–TIMI 36 (Metabolic Efficiency With Ranolazine for Less Ischemia in Non–ST-Elevation Acute Coronary Syndrome–Thrombolysis In Myocardial Infarction 36) Trial

OBJECTIVES The purpose of this study was to assess the relationship between ischemia detected on continuous electrocardiographic (cECG) recording and cardiovascular outcomes after acute coronary syndrome (ACS). BACKGROUND The small size of prior studies evaluating cECG prevented full evaluation of the risk associated with ischemia across subpopulations and compared with other methods of risk stratification. Ranolazine, a new antianginal agent, reduces ischemic symptoms in patients with chronic angina and after ACS but the anti-ischemic effect, as detected by cECG, is not known. METHODS In all, 6,560 patients hospitalized with non-ST-segment elevation ACS were randomly assigned to ranolazine or placebo in the MERLIN-TIMI 36 (Metabolic Efficiency With Ranolazine for Less Ischemia in Non-ST-Elevation Acute Coronary Syndrome-Thrombolysis In Myocardial Infarction 36) trial. The cECG was performed for 7 days after randomization. Outcomes were followed for a median of 348 days. Clinical events that occurred during cECG recording were excluded from analysis. RESULTS A total of 6,355 (97%) patients had cECG recordings evaluable for ischemia analysis. Patients with >or=1 episode of ischemia on cECG (n = 1,271, 20%) were at increased risk of cardiovascular death (7.7% vs. 2.7%, p < 0.001), MI (9.4% vs. 5.0%, p < 0.001), and recurrent ischemia (17.5% vs. 12.3%, p < 0.001). The relationship with cardiovascular death was independent of baseline characteristics or elevated biomarkers (adjusted hazard ratio: 2.46, p < 0.001). Ischemia on cECG was associated with significantly worse outcomes in several subgroups. Ranolazine did not reduce the rate of ischemia detected on cECG (19.9% vs. 21.0%, hazard ratio: 0.93, p = 0.21). CONCLUSIONS In more than 6,300 patients with ACS, ischemia detected on cECG occurred frequently and was strongly and independently associated with poor cardiovascular outcomes, including cardiovascular death. Continuous ECG monitoring to detect ischemia after ACS may help to identify patients at increased risk. (Metabolic Efficiency With Ranolazine for Less Ischemia in Non-ST Elevation Acute Coronary Syndromes [MERLIN]; NCT00099788).