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Background: Computed Tomography Angiography (CTA) is a new and promising type of imaging to evaluate cardiac structure and function. Although it does require injection of contrast material and some radiation exposure, it is much less invasive than conventional catheter based on angiography. It has been already shown to correlate well with echocardiography images, but normative values have yet to be established. Objectives: To publish the first known data on CTA measurements for all four chambers of the heart. Methods: We conducted a retrospective chart review study of around 3000 patients over a three-year period (2006-2008) from a private cardiology practice in Phoenix, Arizona. Patients were screened for any preexisting conditions that might contribute to abnormal cardiac structures. A “normal” population of 226 patients’ CTA’s was reviewed and 29 different measurements were taken cardiac anatomy. Patients were then categorized based on sex and BMI and the cardiac measurements were compared. Results: The values obtained were similar to already established normal measurement values from echocardiography. There was good correlation between body mass index (BMI) and the sexes. Conclusion: This study serves to establish normative data for cardiac CTA while also proves to show good correlation with already established normative values for echocardiography and justifies these CTA measurements as an alternative means of cardiac evaluation. Further study regarding the variations between data for specific measurements will be addressed in future studies.

BACKGROUND: While certain P‐Wave morphologies have been associated with abnormal atrial size and either pulmonary or cardiovascular (CV) disease, their relationship to mortality and specific cause of death has not been reported. METHODS: Analyses were performed on the first digitally recorded electrocardiogram (ECG) on 43 903 patients at the Palo Alto Veterans Administration Medical Center since 1987. After appropriate exclusions, 40 020 patients remained. Using computerized algorithms, P‐wave amplitude and duration in 12 leads as well as several standardized ECG interpretations were extracted. The main outcome measures were pulmonary and CV mortality. RESULTS: During a mean follow‐up of 6 years there were 3417 CV and 1213 pulmonary deaths. After adjusting for age and heart rate in a Cox regression model, P‐wave amplitude in the inferior leads was the strongest predictor of pulmonary death (hazard ratio [HR]: 3.0, 95% confidence interval [CI]: 2.3–3.9, P < .0001 for an amplitude > 2.5 mm), outperforming all other ECG criteria. The depth of P‐wave inversion in leads V(1) or V(2) and P‐wave duration were strong predictors of CV death (HR: 1.7, 95% CI: 1.5–2.0, P < 0.0001 for a P‐wave inversion deeper than 1 mm), outperforming many previously established ECG predictors of CV death. CONCLUSIONS: P‐wave amplitude in the inferior leads is the strongest independent predictor of pulmonary death while P‐wave duration and the depth of P‐wave inversion in leads V(1) or V(2) significantly predict CV death. These measurements can be obtained easily and should be considered as part of clinical risk stratification. Copyright © 2010 Wiley Periodicals, Inc.

INTRODUCTION: Many studies have demonstrated that reduced high-density lipoproteins (HDL) levels and elevated triglyceride (TG)/HDL ratio correlate with the development of chronic ischemic heart disease. The role of HDL and the development of cardiac rhythm disturbances in the non-ST segment elevation acute coronary syndrome (ACS) is unclear. HYPOTHESIS: We assessed the hypothesis that HDL might be protective against development of cardiac rhythm disturbances. Additionally, any protective effect was compared with TG/HDL and LDL/HDL in this setting. METHODS: A total of 6881 patients who presented during 2000–2003 with non-ST segment elevation ACS had fasting lipid panels collected within the first 24 hours of admission. Patients were followed for the development of rhythm disturbances of up to 6 years after initial presentation, with a mean of 1269 days. These patients were further separated into diabetic and nondiabetic groups. RESULTS: After adjustment for ischemic heart disease, congestive heart failure, stroke, peripheral vascular disease, hypertension, low density lipoprotein cholesterol, triglycerides, age, and body mass index, higher HDL levels were found to be independently protective against developing atrial fibrillation and other cardiac rhythm disturbances. TG/HDL and LDL/HDL were also protective of cardiac arrhythmias but not with the same power as low HDL (HDL > 31mg/dl, HR = 3.69, 95% CI=3.01– 4.53, P < 0.05). CONCLUSIONS: Based on the above results, patients with lower HDL levels during hospitalizations with non-ST segment elevation ACS have a greater chance of developing cardiac rhythm disturbances independent of other risk factors. Although higher TG/HDL and LDL/HDL are also predictive, lower HDL is associated with highest OR for the development of cardiac arrhythmia among diabetic and non-diabetic patients with non-ST elevation with ACS.

The Video Atlas of Two-Dimensional Color Flow Doppler Echocardiography by George M. Gura, Jr, MD, consists of a 180-page book and two videocassettes with a total running time of 2 1/2 hours. The quality of the text and software is superb. Indeed, these are the finest color Doppler images that have been produced for teaching in either the printed atlas or tape format to date. It is obvious that much forethought went into the preparation of the material, binding of the book, photographic technique, and packaging of all contents. Great care was taken to ensure that the text and video would be complementary without appearing repetitious. Additionally, the reader is presented with consistent left-to-right orientation of the book's descriptions and figures. In this fashion, the pages need not be turned in order to appreciate the illustrations. The author presents the material in a concise, orderly fashion, and subjects include valvular

Standard 12 lead electrocardiograms (ECG) and Frank vectorcardiograms (VCG) were recorded in 21 consecutive patients with mitral valvular disease and angiographically documented left atrial enlargement. Comparative sensitivities for the detection of left atrial enlargement were: diagnostic, ECG = 6/21 (29%), VCG = 14/21 (67%); suggestive, ECG = 3/21 (14%), VCG = 2/21 (9%); non-diagnostic, ECG = 12/21 (57%), VCG = 5/21 (24%). It is concluded that the Frank atrial vectorcardiogram is superior to the standard electrocardiogram for the diagnosis of left atrial enlargement.

Six months after lumbar disc surgery, a 43-year-old woman presented with signs and symptoms of high-output circulatory failure secondary to an acquired abdominal arteriovenous fistula. Unusual findings in this case included a continuous murmur, which was transmitted to the soles of both feet and pericardial effusion, both of which disappeared after corrective surgery. Echocardiography demonstrated resolution of chamber enlargement following repair of the fistula. The mechanism of vascular injury during disc surgery and hemodynamic effects of such A-V fistulas are discussed.

Fifty consecutive patients were referred to the noninvasive laboratory for evaluation of suspected peripheral vascular disease. There were 30 men and 20 women aged 27 to 88 years (mean 63). Measurement of cardiovascular risk factors revealed the following distributions: cigarette smoking 90 percent, hypertension 28 percent, diabetes mellitus 22 percent and hyperlipidemia 6 percent. Eight patients had a history of angina pectoris, 7 a prior myocardial infarction, 5 a cerebrovascular accident and 11 prior peripheral arterial revascularizatlon surgery. Evaluation detected 32 patients (64 percent) with occlusive arterial disease of the lower limbs. Lead II of the electrocardiogram was monitored during and 1, 2, 3, 4, and 5 minutes after treadmill exercise with a limiting grade of 10 percent at 2.5 miles/hour. The mean resting and maximal heart rates for the study group were, respectively, 78 and 106 beats/min. The average treadmill speed attained was 1.9 miles/hour at a mean duration of 3.8 minutes. Thirty-seven subjects (74 percent) had normal electrocardiographic responses to exercise. Of 13 patients (26 percent) with an abnormal exercise electrocardiogram, 7 had possible ischemic S-T segment responses. Six subjects manifested frequent premature ventricular complexes during exercise. Four other patients had abnormal S-T segments in the resting electrocardiogram (two had a pattern of left bundle branch block, and two a pattern of left ventricular hypertrophy and strain). A survey of 60 peripheral vascular laboratories in the United States revealed that only 29 percent of the responding 34 centers routinely performed electrocardiographic monitoring during exercise testing. It is concluded that (1) electrocardiographic monitoring during exercise in the peripheral vascular laboratory can provide useful information regarding S-T segment responses, (2) abnormal S-T segment responses in patients with suspected peripheral vascular disease are frequently manifested at low levels of work load, and (3) such routine monitoring should be performed for patient safety.

A prospective study of 182 patients undergoing cardiac surgery was performed. The patients were divided into three groups. Group I consisted of 83 patients who had never been treated with digitalis. Group II comprised 59 patients who were taking digoxin before operation and had medication discontinued 24 to 48 hours prior to surgery; they did not receive maintenance digoxin in the postoperative periods. Group III was made up of 40 patients who were given prophylactic digoxin in the perioperative period; none had taken digoxin before. Sixty of 83 group I patients (72%) and two of the group III patients (5%) developed postoperative supraventricular tachyarrhythmia. Digoxin was reinstituted in 56 of group II patients (95%) for supraventricular arrhythmia and/or heart fallure. Of the various factors evaluated, only valvular surgery and ECG evidence of myocardial infarction were associated with postoperative supraventricular tachyarrhythmias.

A 47-year-old man experienced palpitations and shortness of breath following push-up exercises. Because of paroxysmal atrial fibrillation and fatigue, the patient underwent investigation. Echocardiography and cardiac catheterization indicated the diagnoses of mitral valve prolapse and rupture of the chordae tendineae. This report represents the first description of such a sequence of events.

A 61-year-old man had progressive dys pnea along with signs and symptoms sug gesting severe right heart failure following aortocoronary bypass surgery. He was ini tially treated with indomethacin, digoxin, and furosemide, but with no major change in his condition. Four months after opera tion the patient presented with clinical find ings compatible with the postpericardiotomy syndrome and hemodynamic evidence of constriction. Pericardiectomy resulted in a marked improvement in his functional ca pacity. The possible mechanism for peri cardial constriction following open heart surgery is discussed.

The sequence of events in this case suggests that mitral valve prolapse may be an underlying cause of 'athlete's heart syndrome,' especially when it's accompanied by symptomatic arrhythmias.

Selective aortocoronary bypass graft angiography was performed in 30 postoperative subjects. Thirty-one of 39 patent graft injections resulted in cardiac arrhythmias including sinus bradycardia, premature ventricular depolarizations, sinoatrial arrest and atrioventricular (A-V) block. In contrast, only 2 of 39 graft angiograms performed during right atrial pacing produced arrhythmias. We conclude the following: (1) Routine prophylactic right atrial pacing is a valuable method for preventing certain cardiac arrhythmias during aortocoronary graft opacification; and (2) the potential for rapid institution of right ventricular pacing provides safety in the event that angiographically induced A-V block occurs.

The phonocardiographic characteristics of the porcine bioprosthesis in the aortic position were evaluated in 24 asymptomatic patients. A medium to high frequency early systolic sound (AO) was present in 16 of 24 patients; abrupt "halting" of the stiff cusps of the porcine bioprosthesis during early left ventricular ejection seems to be the likely mechanism for the genesis of this sound. An unusually high amplitude aortic closing sound (AC) was present in all patients. A high frequency crescendo-decrescendo systolic murmur in early to mid systole was present in 22 patients. Possible mechanisms for the systolic murmur include: 1) altered resonating properties of the cusps, 2) functional bioprosthetic stenosis, and 3) the presence of a flexible stent. An early systolic opening sound preceding a short systolic murmur and a loud closing sound are common phonocardiographic findings of an uncomplicated porcine bioprosthesis in the aortic position. Therefore, absence of the aortic opening sound, alterations in the amplitude of the aortic closing sound, or an increase in the length of the systolic murmur may suggest bioprosthetic malfunction.

Thirty-two patients from a larger series of subjects undergoing routine postoperative evaluation of the aortocoronary saphenous bypass graft procedure were found to have one (20 patients) or all (12 patients) of the implanted grafts totally occluded. Such occlusion occurred in association with persistent postoperative subjective improvement manifested by a significant diminution or complete disappearance of angina pectoris. Postoperative myocardial infarction was documented in only seven cases, and the possibility of successful partial revascularization could be logically applied to only 20 of these 32 patients. Other suggested mechanisms for relief of angina pectoris in this setting are mentioned, although none is scientifically proved. It is concluded that (1) the marked subjective improvement documented in this population does not universally correlate with anatomic success and that (2) a diminution in the degree of angina pectoris cannot be clinically applied as a reliable indicator of postoperative graft patency.

With the use of a Doppler flowmeter catheter, phasic instantaneous aortocoronary saphenous vein bypass graft blood velocity was continuously measured during the inhalation of amyl nitrite in 20 closed-chest conscious subjects. Administration of amyl nitrite augmented peak diastolic and systolic graft blood velocity within 10 seconds and maximal blood velocities were recorded between 8 and 60 seconds after inhalation. Control mean (+/- 1 S.D.) bypass graft blood velocity was 25 +/- 10 cm. per second and after amyl nitrite 46 +/- 14 cm. per second, resulting in an average 84 per cent rise of blood velocity. It is concluded that amyl nitrite increases aortocoronary bypass graft blood velocity, suggesting a possible enhancement of blood flow to the distal native circulation in patients so operated upon.

With the use of the Doppler ultrasonic catheter telemetry system, phasic left coronary blood velocity was measured in 34 conscious subjects during transvenous pacemaker insertion and right ventricular endocardial pacing. Ventricular premature depolarizations and ventricular tachycardia, occurring as consequences of pacing catheter manipulation and competitive rhythms, reduced peak coronary blood velocity by approximately one half. These findings provide insight into the genesis of sudden death associated with pacemaker insertion, competitive or repetitive arrhythmias, and pacemaker “runaway.”

Pre- and postoperative hemodynamic indices were compared in 116 patients subjected to aorto-coronary bypass after an average interval of 128 days. The patients were separated into three different groups according to graft status: Group 1 (n = 77), all grafts patent; Group 2 (n = 27), one occluded graft out of two or three implanted; Group 3 (n = 12), all grafts occluded. There were no significant major changes of values so obtained in the three groups. Those subjects with initially depressed cardiac indices or elevated left ventricular end-diastolic pressures manifested a significant trend toward improvement when at least one bypass graft was patent. A reduction of cardiac index was noted in patients with occluded left anterior descending coronary grafts only in association with closure of other grafts. Deterioration of cardiac index or left ventricular end-diastolic pressure into the abnormal range was unusual in the study group, even when all grafts were occluded. It is concluded that data relating to the influence of aorto-coronary bypass on standard indices of left ventricular function can be properly interpreted only when certain subsets of patients are studied.

A case of Coxsackie B5 viral myopericarditis is presented in which the diagnosis of inferolateral wall myocardial necrosis was made on the basis of specific cardiac enzyme changes and radionuclide myocardial imaging. This localized damage may have resulted from coronary arteritis with resulting infarction or necrosis secondary to preferential viral involvement of the inferolateral wall of the myocardium. Hepatitis and cerebral embolism complicated the case, with the latter suggesting endocardial disease.

Echocardiography was performed in 25 consecutive patients with angina pectoris and angiographically demonstrable coronary artery disease. Left ventricular echograms detected late or pansystolic mitral valve bowing suggesting of mitral valve proplapse in 6/25 (24%). Left ventricular angiography showed prolapse of the posterior mitral leaflet in 15/25 (60%), including 5 detected by echocardiography. Significant triple vessel coronary disease was present in 11 of 15 patients with prolapsed mitralvalve. In each of the latter a greater than 90 per cent obstructive lesion was noted in at least one coronary artery: right coronary artery, 9 subjects (82%); left circumflex coronary artery, 5 patients (33%); and left anterior descending coronary artery, 4 patients (27%). Of 15 subjects with angiographic evidence of mitral valve prolapse, 13 had left ventricular asynergy-inferior or inferoposterior in 8 subjects (62%) and anterior or anteroapical in 5 subjects (38%). Eleven subjects had vectorcardiographic evidence of transmural myocardial infarction-inferior or inferoposterior in 9 (82%) and anteroseptal in 2 (18%). A single subject with mitral valve prolapse had mild mitral regurgitation. It is concluded that: (1) coexisting prolapse of the posterior mitral valve leaflet and coronary artery disease is usually associated with triple vessel obstructive lesions, (2) severe right coronary disease, inferior left ventricular wall asynergy, and inferior myocardial infarction are important angiographic and vectorcardiographic correlates, and (3) echocardiography will detect such mitral valve prolapse in only one-third of affected cases.

With use of the Doppler ultrasonic flowmeter catheter telemetry system, blood flow velocity was recorded from various left ventricular cavity sites in 57 conscious subjects with atrial arrhythmias. Premature atrial depolarizations reduced peak left ventricular blood flow velocity in direct relation to their respective coupling intervals. Paroxysmal supraventricular and multifocal atrial tachycardias produced a decrease in peak left ventricular blood velocity, with the most marked reductions measured at the onset of the tachyarrhythmias. Atrial flutter and fibrillation resulted in midcavity and inflow tract diastolic blood velocity waves that were inscribed in conjunction with atrial depolarizations seen on the simultaneously recorded electrocardiogram. Irregular ventricular responses and changing atrioventricular conduction ratios produced marked irregularity of peak flow velocity. These findings provide the first comprehensive description of left ventricular blood flow velocity during atrial arrhythmias in man.

Echocardiograms and left ventricular angiograms were systematically studied in 20 consecutive patients with hemodynamically proven mitral stenosis who were in sinus rhythm. "Definite" mitral valve prolapse was present on the echograms of 9 of 20 patients (45%), while "possible" mitral valve prolapse was noted on the echograms of 7 of 20 (35%). Of the 9 subjects with definite mitral valve prolapse, 4 had angiographic evidence of this diagnosis and an identical number had mitral regurgitation; 1 patient had both prolapse and mitral regurgitation. No subject with "possible" ultrasonic prolapse or normal systolic mitral valve motion had angiographic mitral valve prolapse. It is concluded that (1) signs of mitral valve prolapse are frequently encountered on the echocardiograms of patients with hemodyn amically proven mitral stenosis who are in sinus rhythm, and (2) when stringent criteria for the echographic diagnosis of prolapse are employed, approximately 50% of affected subjects have concomitant mitral insuffi ciency.

Echocardiograms were recorded in six patients with calcification of the mitral annulus. Echocardiographic sweep from the aorta to the left ventricular cavity revealed dense echoes, representing annulus calcification, posterior to the mitral valve. Characteristic calcium deposits in the region of the mitral annulus were detected on the chest roentgenogram of only a single subject. Cardiac fluoroscopy fluoroscopy demonstrated calcified mitral annulus in all patients. In one patient, coexisting calcified mitral annulus and proven pericardial effusion were diagnosed echocardiographically. It is concluded that the echocardiogram represents a useful noninvasive technic for the diagnosis of calcified mitral annulus.

Summary Standard 12 lead electrocardiograms(ECG) and timed Frank vectorcardiograms (VCG) were recorded in 53 subjects with atrial fibrillation. Thirty-eight patients had echocardiographically documented left atrial enlargement (>4.0 cm) and 15 patients had normal atrial dimensions. The magnitude of the largest “f” wave component during an average cycle length was measured in lead V 1 of the ECG and the horizontal plane VCG running loop. Relative sensitivities for detection of left atrial enlargement were: VCG, 25/38 (66%) and ECG 10/38 (26%). An enlarged left atrial internal dimension was diagnosed by the VCG alone in 21 of the 38 subjects (55%). In the group of 15 patients with normal echocardiographic left atrial internal dimensions the prevalence of ECG false positive diagnosis for enlarged left atrial size was 6% in contrast with 0% for the VCG. It is concluded that: 1) the timed Frank VCG is superior to the ECG for the detection of echocardiographically demonstrable left atrial enlargement; 2) the timed VCG and ECG represent complementary techniques for identifying patients with abnormally large left atria; and 3) large fibrillatory waves are rarely observed on the ECG or VCG when the left atrial internal dimension is echographically normal.

Nineteen subjects with a total of 33 aorto-coronary saphenous vein bypass grafts were subjected to coronary and bypass graft angiography an average of 102 days after operation. There was a significant progression of coronary artery disease in both bypassed and nonbypassed coronary arteries. Net progression of disease was similar in both bypassed (16 ± 12 per cent) and nonbypassed (12 ± 24 per cent) coronary arteries (p > 0.4). There was no significant difference between the mean net progression of disease in coronary arteries with patent grafts (16 ± 12 per cent) and those arteries with nonpatent grafts (16 ± 13 per cent) (p > 0.8). We conclude that the progression of coronary arterial disease in patients subjected to the saphenous vein bypass procedures is a manifestation of the natural history of coronary artery disease and is rarely influenced per se by graft implantation.

The electrocardiograms (ECG) of 64 subjects who exhibited an echocardiographically demonstrable increase in thickness of the interventricular septum and left ventricular posterior wall (Group 1, 22 patients), isolated left ventricular internal dimension (Group 2,26 patients), combined wall thickness and chamber diameter (Group 3, 2 patients), and septal thickness, (Group 4, asymmetric septal hypertrophy, 14 patients) were reviewed in order to determine sensitivity of ECG criteria for the diagnosis of left ventricular hypertrophy (LVH) proposed in 1949 by Sokolow and Lyon (13), in 1968 by Romhilt and Estes (14), and in 1973 the New York Heart Association (15). Relative sensitivity of the three methods was as follows: Total group, NYHA (77%) greater than Sokolow and Lyon (67%) greater than Romhilt and Estes (58%); Group 1, NYHA (91%) greater than Sokolow and Lyon (73%) greater than Romhilt and Estes (54%); Group 2, NYHA and Sokolow and Lyon (65%) greater than Romhilt and Estes (61%); Group 4, NYHA (79%) greater than Sokolow and Lyon (64%) greater than Romhilt and Estes (57%). We conclude that 1)ECG criteria of the NYHA for the diagnosis of LVH correlate best with an increase of ultrasonically determined septal, left ventricular posterior wall or left ventricular internal dimensions when compared with voltage criteria of Sokolow and Lyon and the point score system of Romhilt and Estes; and 2) isolated increase of left ventricular internal dimension, in the absence of thickened septum or posterior left ventricular wall, frequently results in ECG criteria compatible with the diagnosis of LVH.

With use of the Frank lead system, still loop and timed vectorcardiograms were recorded in more than 5,000 patients subjected to complete right and left heart catheterization and selective coronary cineangiography. Data so obtained demonstrated clinical superiority of the vectorcardiogram over the standard 12 lead scalar electrocardiogram. Specific advantages of the vectorcardiogram include (1) recognition of undetected atrial and ventricular hypertrophy, (2) greater sensitivity in identification of myocardial infarction, and (3) superior capability for diagnosis of multiple infarctions in the presence of fascicular and bundle branch blocks. The timed biplane vectorcardiogram is as useful as any number of simultaneously recorded electrocardiographic leads for the analysis of complex arrhythmias and beat to beat changes in intraventricular conduction. Since the validity and usefulness of this technique have been established, it should become part of the routine noninvasive evaluation of patients with cardiovascular disorders.

Summary Distribution of the initial 10–30 msec QRS forces was determined on the Frank vectorcardiograms (VCGs) of 31 patients with complete left bundle branch block (LBBB). Of nine patients with coronary artery disease, three had all 10–30 msec vectors directed posteriorly in the horizontal plane (HP) and associated inferior or apical left ventricular asynergy. Frontal plane initial 30 msec QRS forces were oriented superiorly in two of these three subjects. In five patients with isolated anterior wall myocardial infarction, the HP 10 msec QRS vectors were anterior, followed by posteriorly directed 20–30 msec QRS vectors. Twelve patients with primary cardiomyopathy had initial QRS vectors distributed as follows: 10–30 msec posterior and left in two; 10–20 msec anterior and left in five; 10 msec anterior and left with the 20–30 msec posterior and left in four. In one patient the 10 msec was posterior and right, and 20–30 msec posterior and left. Of 10 patients with valvular heart disease three manifested posterior 10–30 msec QRS vectors. In four the 10 msec vector was anterior and left and 20–30 msec posterior and left. The 10–20 msec were anterior and left and 30 msec posterior and left in two subjects. There was no correlation between posteriorly directed initial QRS forces and left ventricular hypertrophy in the latter group. We conclude that: 1) posterior orientation of the initial 10 msec QRS vectors in the presence of LBBB is not specific for myocardial infarction; 2) when present in patients with obstructive coronary artery disease such abnormal posterior forces correlate with anterior and probable co-existing infero-apical infarction and, 3) factors aside from left ventricular hypertrophy can produce abnormally directed initial 10–30 msec QRS vectors in subjects with valvular heart disease.

Left ventricular function was noninvasively assessed by echocardiography, and left ventricular ejection time index (LVETI) was derived from external carotid pulse tracings in 25 patients before (B) and an average of 17 days after (A) Hancock porcine valve implantation. Fifteen patients had aortic valve replacement and 10 had mitral valve replacement; 4 had a combined procedure. In the aortic and combined group, (n = 15) there were significant (P < 0.0025) changes of mean (± 1 SD) left ventricular end-systolic dimension (ESD), B = 5.1 ± 0.9, A = 4.3 ± 0.9 cm; end-diastolic dimension (EDD), B = 5.7 ± 1, A = 4.9 ± 0.9 cm; mean rate of circumferential fiber shortening (VCF), B = 0.37 ± 0.05, A = 0.75 ± 0.04 circumf/sec and LVETI, B = 0.45 ± 0.05, A = 0.39 ± 0.02 sec. In subgroups with preoperative aortic stenosis (n = 8), combined aortic stenosis and insufficiency (n = 3), and coexisting aortic and mitral disease (n = 4), there was a uniform reduction of ESD, EDD, and LVETI with an increase of VCF. In the isolated mitral valve replacement group (n = 10), the values were ESD (B = 4.6 ± 0.7, A = 4.4 ± 0.8 cm, P = not significant); EDD (B = 5.2 ± 0.6, A = 4.7 ± 0.8 cm, P < 0.0025); VCF (B = 0.36 ± 0.08, A = 0.7 ± 0.04 circumf/sec, P < 0.0025); and LVETI (B = 0.40 ± 0.03, A = 0.37 ± 0.03 sec P < 0.05). Patients with mitral stenosis (n = 2), mitral insufficiency (n = 3), and combined mitral stenosis and insufficiency (n = 5) all had a postoperative decrease in ESD, EDD, and LVETI with augmentation of VCF. We concluded that (1) early noninvasive assessment of left ventricular function after Hancock valve implantation indicates a significant hemody namic improvement, and (2) echocardiography combined with external ca rotid arterial pulse tracing analysis is useful for the follow-up of patients who receive Hancock valves.

Utilizing a Doppler ultrasonic flowmeter catheter, phasic instantaneous aortocoronary saphenous vein bypass blood velocity was recorded during various atrial arrhythmias in 17 patients. Atrial premature beats, supraventricular tachycardia and atrial fibrillation reduced peak bypass graft blood velocity in relation to the heart rate and diastolic cycle length. Such changes were more evident during the systolic fraction of bypass blood flow. In a single subject, systolic blood velocity alternans was observed during the course of atrial tachycardia. It is concluded that such study provides insight into the dynamics of bypass graft blood flow velocity during atrial arrhythmias.

A 54-year-old woman underwent re placement of a thrombosed Björk-Shi ley aortic valve prosthesis. Post oper ative electrical defibrillation resulted in isolated T wave alternation which progressed to total QRS-T electrical al ternans. This report represents the first description of such a phenomenon.

Echocardiography was performed in 28 consecutive patients who manifested accepted criteria for left ventricular hypertrophy on their electrocardiograms. Four groups of patients were identified: Group 1, nineteen (68%) who had an increase in both interventricular septal and left ventricular posterior wall thickness; Group 2, three patients (11%) with isolated enlargement of the left ventricular internal dimension; Group 3, two subjects (7%) with increased septal thickness, left ventricular posterior wall thickness and left ventricular internal dimension and Group 4, four patients (14%) with normal echocardiographic measurements. It is concluded that increases in both septal and left ventricular wall thickness are the primary echocardiographic correlates of left ventricular hypertrophy as diagnosed on the electrocardiogram.

Forty-four consecutive patients who had perfusion defects on thallium-201 scanning and positive exercise treadmill tests were prospectively studied. Thirty-eight (86%) subjects had diagnostic ST segment changes in lead V5, 37 (84%) in lead V4, and 44 (100%) in either lead V4, V5 or both. Thirty patients had ST segment changes in the inferior leads, 20 in lead aVR, and only four in lead I and/or aVL. All of these latter subjects had diagnostic ST segments in lead V4 and/or V5. It is concluded that: combined electrocardiographic leads V4 and V5 detect the vast majority of ischemic changes during exercise treadmill testing, regardless of the site of perfusion defects detected by thallium-201 scanning; and monitoring the inferior and lateral leads rarely provides more diagnostic information.

By means of the Doppler ultrasonic flowmeter catheter, phasic instantaneous left ventricular blood velocity was measured at the mitral valves of 184 conscious human subjects during atrial arrhythmias. Atrial extrasystoles and pacemaker-induced atrial tachycardias reduced peak mitral valve blood velocities in direct relation to shortened diastolic cycle length. Atrial fibrillation with irregular ventricular responses produced beat-to-beat alterations of peak mitral blood velocity, with smaller peak mitral blood velocities usually associated with shortened R-R intervals on the electrocardiogram. This report represents the first comprehensive description of instantaneous and continuous phasic blood velocity at the mitral valve during atrial arrhythmias in man. It is concluded that atrial tachyarrhythmias exert an adverse influence on left ventricular filling velocities.

Phasic instantaneous aortocoronary bypass graft blood flow velocity was measured with the Doppler flowmeter catheter in 12 conscious postoperative patients. Graft blood flow velocity is characterized by a large diastolic component with a smaller systolic fraction. Values for systolic flow velocity were uniformly greater at the graft origins when compared with similar measurements at the ostia of bypassed coronary arteries. Graft blood flow velocity decreased in a few subjects who experienced ventricular dysrhythmias. In two patients, inhalation of amyl nitrite resulted in augmented graft blood flow velocity. We conclude that the Doppler flowmeter catheter technique is useful for the direct measurement of aortocoronary bypass graft blood flow velocity in a variety of normal and pathologic states in closed chest conscious subjects.

Using the Frank lead system, the Vectorcardiographic features of coexisting left anterior hemiblock and inferior wall myocardial infarction were characterized in 25 patients. The Vectorcardiographic findings most useful for the diagnosis of coexisting left anterior hemiblock and inferior myocardial infarction are: Frontal plane: (1) clockwise and superior inscription of the 20 to 30 msec QRS vectors, (2) counterclockwise and delayed inscription of the terminal 40 msec QRS vectors, (3) maximal QRS deflection vector located in the left superior quadrant, and (4) major area of the QRS loop above the X axis. Sagittal plane: (1) superior inscription of the 20 to 30 msec QRS vectors, (2) deviation of the maximal QRS deflection vector superiorly and posteriorly, (3) delay in inscription of the terminal 40 msec QRS vectors, and (4) figure-of-eight or counterclockwise rotation of the QRS loop. Because of the difficulties in the electrocardiographic recognition of coexisting left anterior hemiblock and inferior myocardial infarction, utilization of the Frank vectorcardiogram appears to be a superior means for diagnosis.

Instantaneous and continuous measurement of phasic blood flow velocity was obtained with the Doppler ultrasonic flowmeter system in over 700 patients. Using transcutaneous and implanted probes, flow velocity was recorded from arteries in normal subjects and patients with aortic valvular and subvalvular disease, arrhythmias, myocardial infarction and congestive heart failure. Catheter probe recordings were obtained from the superior vena cava, right atrium, right ventricle, aorta, carotid arteries and coronary arteries in patients with a variety of clinical disorders. Ventricular diastolic and atrial systolic flow in atrial septal defect, compensatory diastolic flow acceleration in tricuspid insufficiency, peak flow velocity variations dependent on previous cycle length in arrhythmias, small atrial contribution to ventricular systolic flow, diagnostic recognition of aortic valvular disease, and other flow velocity relations are stressed.

Simultaneous leads I, II, and III of the electrocardiogram were recorded during selective aortocoronary saphenous vein bypass graft angiography in 20 patients. Arrhythmias associated with such graft opacification included sinus bradycardia, sinus arrest, atrial premature beats, ventricular premature beats, ventricular tachycardia and two episodes of ventricular fibrillation. Rhythm disturbances were unrelated to the anatomic location of the grafts. Patent right graft injection effected a mean rightward frontal plane QRS axis shift of 32.7 ° with leftward T wave axis deviation. A majority of subjects with patent aortic-left anterior descending coronary arterial grafts also manifested right axis shift (mean 22.6 °), possibly related to collateral circulation between the left and right coronary arterial systems. Those patients with stenosed and occluded grafts had minimal or no electrocardiographic changes during bypass angiography. It is concluded that electrocardiographic alteration during graft angiography is a physiologic demonstration of aortocoronary bypass efficacy.