Improved detection of posterior myocardial wall ischemia with the 15-lead electrocardiogram.

BACKGROUND: A routine 12-lead electrocardiogram is commonly obtained to evaluate for possible acute myocardial infarction during the initial screening of patients with chest discomfort. Posterior myocardial infarction is commonly missed because it is not usually visible in the standard leads. In this study, we compared the sensitivity and specificity of posterior chest leads (V(7), V(8), and V(9)) and 12-lead electrocardiography in detecting posterior injury pattern during single-vessel percutaneous transluminal coronary angioplasty. METHODS AND RESULTS: Three posterior chest leads in addition to the routine 12-lead electrocardiogram were monitored simultaneously during single-vessel percutaneous transluminal coronary angioplasty of the right, circumflex, and left anterior descending coronary arteries in a total of 223 patients. Posterior injury patterns (95%) were detected mostly during circumflex coronary occlusion. Posterior leads were able to detect injury pattern in 49% (36 of 74) of patients, whereas the 12-lead electrocardiogram was able to detect only 32% (P <.04). When all 15 leads were used to detect all ST elevations, sensitivity increased to 57%, with a specificity of 98% for the circumflex coronary artery. If maximal ST depressions in leads V(2) to V(3) are considered to be from posterior myocardial injury, then the overall sensitivity is increased to 69%. CONCLUSIONS: Posterior leads significantly increased the detection of posterior injury pattern compared with the standard 12-lead electrocardiogram. Using all 15 leads significantly further improved the detection of circumflex coronary-related injury pattern over the standard 12-lead electrocardiogram.

Importance of posterior chest leads in patients with suspected myocardial infarction, but nondiagnostic, routine 12-lead electrocardiogram.

Criteria for reperfusion therapy in acute myocardial infarction require the presence of ST elevation in 2 contiguous leads. However, many patients with myocardial infarction do not show these changes on a routine 12-lead electrocardiogram and hence are denied reperfusion therapy. Posterior chest leads (V7 to V9) were recorded in 58 patients with clinically suspected myocardial infarction, but nondiagnostic routine electrocardiogram. ST elevation >0.1 mV or Q waves in > or =2 posterior chest leads were considered to be diagnostic of posterior myocardial infarction. Eighteen patients had these changes of posterior myocardial infarction. All 18 patients were confirmed to have myocardial infarction by creatine phosphokinase criteria or cardiac catheterization. Of the 17 patients who had cardiac catheterization, 16 had left circumflex as the culprit vessel. We conclude that posterior chest leads should be routinely recorded in patients with suspected myocardial infarction and nondiagnostic, routine electrocardiogram. This simple bedside technique may help proper treatment of some of these patients now classified as having unstable angina or non-Q-wave myocardial infarction.

When we "act" on ACT levels: activated clotting time measurements to guide heparin administration during and after interventional procedures.

The establishment and monitoring of anticoagulation before, during, and after interventional and invasive procedures are crucial responsibilities. However, few prospective studies exist to rationally guide us in how and when to "act" in response to ACT values in specific clinical situations. Definitive studies to reach a uniform and safe ++approach are needed. The articles published in this issue of Catheterization and Cardiovascular Diagnosis represent an important step in understanding the role and value of ACT levels.

Adequate heparinization during PTCA: assessment using activated clotting times.

Heparinization during PTCA is often done empirically with an initial 10,000 unit bolus of heparin and subsequent additional boluses as deemed necessary to prevent thrombus formation and fibrin deposition. However, the initial 10,000 unit bolus may not result in adequate systemic anticoagulation in every patient, exposing some patients to risk of thrombus at the angioplasty site and subsequent reocclusion. In this non-randomized study, we assessed systemic coagulation during PTCA by retrospectively analyzing activated clotting times obtained in 108 consecutive patients. All patients had normal baseline prothrombin times and activated partial thromboplastin times. Patients who were on heparin prior to PTCA were excluded. Based on data from studies on heparinization during extracorporeal bypass an activated clotting time (ACT) of greater than 300 seconds was required. Twelve patients (11%) were observed to have activated clotting times of below 300 seconds after an initial 10,000 unit bolus of heparin. These patients required an additional 3,000-10,000 units of heparin to have systemic anticoagulation during PTCA. Symptoms of stable or unstable angina had no significant effect on heparin requirement, although there was a trend toward greater heparin resistance in unstable angina. We conclude that it is important to monitor the status of anticoagulation during PTCA, for 11% of patients undergoing PTCA require additional initial heparin bolus to achieve an ACT greater than 300 seconds and to be effectively anticoagulated. Careful monitoring of heparinization during PTCA may reduce the incidence of thrombosis.

A non-linear elastic model of contraction of ischaemic segments.

Previous studies have characterised the motion of the myocardium using a linear time varying elastance model, ie, they have sought to characterise the relationship between left ventricular volume and internal pressure as linear, but with time varying slopes over the cardiac cycle. However, the motion of myocardium during regional ischaemia has not been characterized by such models. Studies of totally ischaemic tissue and of myocardium in diastole have characterised the relationship between tension or stress and segment length as exponential. It is the purpose of this study to present a new model in which myocardial contraction is expressed as an exponential, but time varying elastic relationship. In this model tension, T, is related to segment length according to the formula T = e alpha(t)L + beta, where alpha(t) rises with systole and falls in diastole. This model was applied to the motion of hypokinetic segments noted in a series of conscious dogs studied for other purposes. Hypokinetic segments display early systolic bulging, decreased systolic shortening, and early diastolic recoil. These particular types of segment motion are naturally predicted by this model. Furthermore, the motion of myocardial segments as they become increasingly ischaemic may be predicted, including a gradual shift to the right and narrowing of the tension-length loop. alpha was noted to be independent of loading change, and thus may be viewed as an index of contractility. This model thus predicts the pattern of motion of hypokinetic segments and provides new insight into myocardial contractility.

The effect of ionic contrast medium on the movement of acutely ischemic and nonischemic canine myocardium.

Regional function assessed by ventriculography may be influenced by the hemodynamic effects of rapidly injecting ionic contrast medium. The importance of this after acute coronary occlusion was examined in eight open-chest, anesthetized dogs. The left anterior descending artery was ligated while sonomicrometric segment lengths in the ischemic (IZ) and nonischemic zones (NZ) were measured. Sodium methylglucamine diatrizoate (Renografin-76, 1 ml/kg) was rapidly injected over 3 seconds. Fifteen minutes later, the left ventricular end-diastolic pressure (LVEDP) was rapidly increased to the level reached during injection. Injecting the contrast increased the LVEDP (7.3 +/- 2.5 to 20.1 +/- 2.9 mm Hg, p less than 0.0001) to the same extent as raising LVEDP (7.6 +/- 2.5 to 10.1 +/- 2.9 mm Hg, p less than 0.0001). Injecting the contrast medium increased IZ total percent systolic shortening (% delta L) (-3.90 +/- 4.43% to -2.68 +/- 4.77%, p less than 0.001) by decreasing isovolumic bulging (-6.68 +/- 4.09% to -5.49 +/- 3.33%, p less than 0.001) with little change in ejection % delta L. NZ total % delta L tended to increase (19.03 +/- 6.53% to 19.94 +/- 6.27%, p = 0.015) because of augmented ejection % delta L (13.12 +/- 2.51% to 13.71 +/- 3.10%, p = 0.017) by the Starling mechanism. Increasing the LVEDP had the same effect on IZ and NZ regional shortening as injecting contrast. Thus regional shortening after acute coronary occlusion is affected by the changes in loading conditions with ionic contrast ventriculography.(ABSTRACT TRUNCATED AT 250 WORDS)

Surgical revascularization of left main coronary artery stenosis: determinants of perioperative and long-term outcome in the 1980s.

The postoperative courses of 176 patients who underwent coronary artery bypass surgery for significant left main coronary artery stenosis were analyzed to determine which preoperative clinical and angiographic factors correlated best with outcome. Clinical variables included age, sex, New York Heart Association (NYHA) anginal class, presence of unstable angina, and surgical class. The angiographic variables included percentage of left main stenosis, presence of right coronary artery stenosis, coronary dominance, number of vessels diseased, myocardial jeopardy score, and ejection fraction. The overall perioperative mortality rate was 9.1%. There was a significant increase in perioperative mortality among female patients (p less than 0.05) and patients undergoing emergency surgery (p less than 0.05). Patients with left main stenosis of 80% or more or with balanced or left dominant circulation showed trends toward increased perioperative mortality. Life-table analysis showed that emergency surgery and left main stenosis of 80% or more correlated with increased long-term mortality (p less than 0.05). No other variable tested showed a significant correlation with either perioperative or long-term mortality. A comparison of these results with studies performed in the 1970s shows that there has been considerable change in those factors which place a patient at increased risk for mortality during surgical treatment of left main coronary artery stenosis.

Augmentation of contraction in remote nonischemic zone during acute ischemia.

We studied how left ventricular loading conditions and the size of the ischemic zone affect regional segmental shortening (% delta L) in ischemic (IZ) and remote nonischemic zones (NZ) after acute coronary occlusion. Distal and proximal portions of the left anterior descending artery (group I, 10 dogs) or the left circumflex artery (group II, 10 dogs) were occluded in two stages. Segment length sonomicrometers were placed in the distal and proximal IZ and in the distal and proximal NZ. % delta L was divided into isovolumic and ejection phases. Left ventricular end-diastolic pressure (LVEDP) was decreased 3 +/- 1 mmHg by blood withdrawal and then increased 6 +/- 2 mmHg by blood transfusion before and after distal and proximal coronary occlusions. LVEDP was brought back to its initial value before distal and proximal coronary occlusions. Regional blood flow and total blood flow deficit were measured with microspheres. Similar results were obtained in group I and II experiments. After coronary occlusion, the IZ showed systolic bulging occurring primarily in isovolumic systole. In the NZ, total and isovolumic % delta L increased from control, whereas ejection % delta L did not change. As LVEDP was raised, IZ isovolumic bulging decreased and ejection % delta L was unchanged, whereas NZ isovolumic % delta L decreased and ejection % delta L increased. Thus IZ bulging and NZ isovolumic % delta L changed in opposite directions when load was varied. The larger IZ after proximal coronary occlusion tended to increase the amount of NZ isovolumic % delta L. In conclusion, at low LVEDP NZ augmentation is predominantly caused by an increase in isovolumic % delta L, whereas if LVEDP is increased it is because of an increase in ejection % delta L. In addition, in open-chest animals augmented contraction in the NZ may be related to the size of the IZ.

The resolution of coronary collaterals after successful percutaneous transluminal coronary angioplasty.

It has been shown that collaterals can develop rapidly during acute coronary occlusion, either due to thrombosis or during angioplasty (PTCA). However, the fate of well-developed collaterals immediately after a successful PTCA is unknown. Accordingly, 15 patients with Rentrop class 2 or 3 collaterals as visualized angiographically were studied immediately after successful single-vessel PTCA. The left anterior descending artery contained the stenosis in nine patients and the right coronary contained the stenosis in six patients. There was total occlusion of six vessels and subtotal occlusions of nine vessels pre PTCA. Immediately after PTCA, flow through the collaterals to the stenosed artery could no longer be visualized angiographically in eight patients (group 1), but remained faintly visible in seven patients (group 2). There was no difference between these two groups with regard to pre PTCA transstenotic pressure gradient (46 +/- 12 vs 42 +/- 14 mm Hg), post PTCA pressure gradient (13 +/- 7 vs 11 +/- 10 mm Hg), or post PTCA percent luminal diameter narrowing (26 +/- 18% vs 24 +/- 13%). These findings suggest that despite similar hemodynamic and angiographic improvement, the resolution of collaterals immediately after PTCA is variable.

Quantification of absolute luminal diameter by computer-analyzed digital subtraction angiography: an assessment in human coronary arteries.

Determination of absolute lumen diameters has been shown to be useful in predicting the functional importance of a coronary stenosis. In this study, both single-plane and orthogonal biplane digital subtraction angiograms were obtained in human cadaver coronary arteries. A single absolute diameter was calculated at the site of greatest narrowing in 20 segments by two automated computerized algorithms. Minimum and maximum diameters at the site of the stenosis were measured from pathologic sections prepared after pressure fixation. Method 1, which determines the edges by means of the first derivative of the videodensity curve, derived absolute diameters that fell between the pathologic minimum and maximum in 10 of 20 segments. Method 2, which determines the edges by an average of the first and second derivatives of the videodensity change, derived absolute diameters that fell between the pathologic minimum and maximum diameters in 15 of 20 segments. Method 1 correlated well with the maximum pathologic diameter (r = .76) and less well with the minrmum pathologic diameter (r = .67). Method 2 correlated very well with the maximum pathologic diameter (r = .79) and also correlated well with the minimum pathologic diameter (r = .74). As would be expected, the computerized algorithms tended to overestimate the minimum pathologic diameter and to underestimate the maximum pathologic diameter. In six segments, two orthogonal views were analyzed; no further accuracy was discernible over single-plane determinations. Thus quantitative coronary angiography by digital subtraction angiography is sufficiently accurate to be of use in the measurement of the severity of a coronary stenosis.

Contractile function and reserve during acute ischaemia in the canine lateral border zone.

The hypothesis that there is a lateral border zone with function intermediate to adjacent ischaemic and non-ischaemic tissue was tested in 10 open chest anaesthetised dogs. Four pairs of segment length crystals were placed in parallel so as to span the ischaemic and non-ischaemic zones. Graded occlusion was produced with a screw clamp applied to a carotid to left anterior descending artery cannulation system. Contractile reserve was assessed using postextrasystolic potentiation. A balloon perfusion labelling system was used to label negatively the potentially ischaemic zone and quantify the admixture of ischaemic and non-ischaemic tissue in the lateral border zone, defined by the fraction of normal zone tissue. When the 40 crystal pairs from the 10 dogs were grouped according to fraction of normal zone tissue (FNZT), 13 were in the central ischaemic zone (FNZT less than 0.1), seven were in the border ischaemic zone (FNZT 0.1-0.5), five were in the border non-ischaemic zone (FNZT 0.5-1.0), and 15 were in the non-ischaemic zone (FNZT 1.0). When the lateral border zone is predominantly non-ischaemic tissue, the tissue behaves as though it is non-ischaemic. Segmental shortening before and after postextrasystolic potentiation in the border non-ischaemic zone and non-ischaemic zone did not change with ischaemia. When tissue in the lateral border zone is predominantly ischaemic, it behaves as though it is ischaemic. Segmental shortening decreased in parallel with progressive ischaemia in the border ischaemic zone and ischaemic zone. At total occlusion, segmental shortening in the border ischaemic zone was -2.3(5.9%) and in the ischaemic zone -3.5(3.6)% (NS).(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of changes in afterload on systolic bulging.

It has been previously shown that after acute coronary occlusion, the extent of systolic bulging is dependent on preload and the function of the remote nonischemic myocardium is influenced by the motion of the ischemic myocardium as well as by the loading conditions. To examine the isolated effects of changing afterload on the movement of acutely ischemic and nonischemic myocardium, seven open-chest, anesthetized dogs were paced from the left atrium at a rate of 100 beats/min after crushing of the sinus node. The pulmonary artery was perfused artificially and the left ventricular end-diastolic pressure (LVEDP) was carefully controlled with a right heart bypass system. Twenty minutes after occlusion of the left anterior descending artery, the peak left ventricular pressure (LVP) was adjusted to three levels (70, 90, and 110 mm Hg) by blood withdrawal or aortic constriction, while the LVEDP was kept constant (8.3 +/- 2.3 mm Hg). Segment length in the ischemic (IZ) and nonischemic zones (NZ) were measured with sonomicrometers and total, isovolumetric, and ejection systolic shortening (% delta L) were calculated. Changes in left ventricular minor-axis diameter were measured with diameter crystals. Increasing the peak LVP increased the LVP both at aortic valve opening and closing. To keep the LVEDP constant as peak LVP was increased, the cardiac output had to be decreased (p less than .0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Prognosis of symptomatic coronary artery disease in young adults aged 40 years or less.

The clinical course and coronary angiographic features of symptomatic coronary artery disease (CAD) in patients younger than 40 years old are described with particular emphasis on the prevalence of myocardial infarction and the degree of diminished functional capacity. Eighty-five patients with CAD proven by coronary angiography were studied. There were 73 men and 12 women aged 27 to 40 years. Fifty-nine patients presented with acute myocardial infarction, most of whom denied previous chest pain, and 14% (12 patients) presented with less acute chest pain syndromes. Coronary angiography was performed in all patients, and greater than or equal to 70% luminal diameter narrowing was considered significant. Coronary angiographic findings reveal 51% with 1-vessel CAD, 31% with 2-vessel and 19% with 3-vessel. Subsequently, 23 patients had coronary artery bypass graft surgery, 7 underwent angioplasty and 55 were treated medically. Follow-up for a mean of 3 years revealed only 1 death and 4 subsequent hospital admissions for cardiac events. Fifty-three percent of the patients are entirely pain free, and only 4 (5%) have significant symptoms of angina pectoris. Although 15 (18%) are not employed regularly, the remainder work full- or part-time, or plan to work in the near future. These data suggest that the short-term prognosis and functional status of young patients with CAD is excellent.

Magnetic resonance imaging to evaluate patency of aortocoronary bypass grafts.

To assess the efficacy of magnetic resonance (MR) imaging in evaluating graft patency after coronary bypass surgery, 20 patients who had prior surgery (average 5.5 years, range 1.5 to 14) and recent cardiac catheterization because of chest pain were studied. No patient had surgical intervention or change in symptoms in the time interval between catheterization and MR imaging. These 20 patients had a total of 47 grafts, defined as proximal anastomoses: 20 to the left anterior descending or diagonal artery (LAD), 13 to the left circumflex artery marginal branches (LCX), and 14 to the right coronary artery or posterior descending artery (RCA). The patients underwent cardiac and respiratory gated MR scans in a 0.5 tesla magnet with an echo time of 22 msec and two repetitions in a 128 X 256 matrix. In-plane resolution was 2.7 mm. Every patient had a scan in the transaxial plane and some underwent scanning in the sagittal and coronal planes as well. A graft was considered patent by MR when a signal-free lumen was visualized in an anatomic position consistent with that of a bypass graft, had a lumen larger than the native vessels, was seen on more than one slice, and was seen at a level higher than that of the native vessels. If a known graft was not seen it was considered occluded. The scans were interpreted by consensus of two physicians aware of the operative but not the cardiac catheterization data.(ABSTRACT TRUNCATED AT 250 WORDS)

Assessment of coronary artery stenoses by digital subtraction angiography: a pathoanatomic validation.

Automated computer assessment of coronary stenoses from digital subtraction angiographic images comparing geometric and videodensitometric algorithms was performed. Digital subtraction angiograms were acquired on a 512 X 512 X 8 bit pixel matrix at 8 frames/second. Fifteen segments from nine human cadaver coronary arteries, with lesions ranging from 0% to 97%, were analyzed. Hand injections of radiopaque dye were made during the pulsatile infusion of saline solution at physiologic pressures and flows. Individual frames best demonstrating a lesion were digitally magnified and the stenosis was measured; the operator identified only the segment of interest. The artery was then injected with a rapidly hardening gel during the same rate of infusion as that used during image acquisition. Histologic sections were cut at 2 mm intervals after fixation and elastic stains applied. Photographs of the section comparable to the site determined from the angiogram were taken, and hand planimetry by a blinded investigator was performed. There was an excellent correlation between histopathology and videodensitometry (r = 0.93; p less than 0.0001). The two geometric algorithms studied also had very good correlations (r = 0.90 and 0.84) with pathology. Two experienced angiographers, despite excellent agreement with each other, had lower correlations with pathology than any of the three computer algorithms studied (r = 0.79 and 0.83, respectively), although this difference did not attain statistical significance. This in vitro model simulating in vivo conditions validates the use of automated videodensitometric and geometric computer algorithms to interpret coronary angiography and assess severity of stenosis.