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Background: Dobutamine and exercise echocardiography are well-validated modalities used for the evaluation of patients with suspected myocardial ischemia. Patients undergoing dobutamine stress echocardiography (DSE), however, experience less angina, ST-segment depressions, and wall motion abnormalities. Other than the effect on heart rate, the physiologic and volumetric differences between pharmacologic and exercise-induced stress that affect myocardial oxygen demand are not well defined. The aim of this study was to test the hypothesis that in the absence of ischemia, dobutamine reduces left ventricular (LV) volume, wall tension (WTN), and peak systolic stress (PSS) compared with exercise., Methods: Seventy patients without ischemia were prospectively enrolled (35 underwent exercise echocardiography and 35 DSE), and various hemodynamic parameters were measured and LV volumes calculated (using the Simpson and Teichholz formulas). Systolic WTN and PSS were determined at rest and stress., Results: LV end-diastolic volume index fell significantly more with dobutamine than with exercise (-34% vs -9%, P < .0001), as did mean end-systolic volume index (-55% vs -37%, P = .07). Systolic blood pressure increased more with exercise (41 ± 22 vs 1 ± 33 mm Hg, P < .0001), as did cardiac index (2.5 ± 0.7 vs 1.0 ± 0.8 L/min/m(2), P < .0001). Systolic WTN increased with exercise by 24% (P < .0001) but decreased with dobutamine by 18% (P < .0001). PSS increased with exercise by 21% (P < .0001) but decreased with dobutamine by 23% (P < .0001)., Conclusions: The degree of stress achieved with DSE appears to be considerably different than with exercise. DSE produces greater reductions in LV end-diastolic and end-systolic volumes than exercise and decreases rather than increases in WTN and PSS. The lower WTN and PSS were related to both a decrease in LV volume and lower systolic blood pressure with dobutamine. These observations support recommendations favoring exercise stress testing in patients able to exercise and reinforce the notion that high-risk echocardiographic features of ischemia such as stress-induced LV dilatation may be less striking or absent with DSE., (Copyright © 2012 American Society of Echocardiography. Published by Mosby, Inc. All rights reserved.)

We present a case of drug-induced pericardial effusion in a patient with end-stage renal disease. Hypertension is frequent among patients with chronic renal failure and sometimes it is necessary to use agents, like minoxidil. Many papers have reported the association between minoxidil and pericardial effusion, both in dialysis patients and those with normal renal function. These effusions sometimes require drainage because of tamponade, but usually disappear after discontinuation of the drug, which is what happened in our patient. In any patient on dialysis treated with minoxidil, the appearance of pericardial effusion unresponsive to ultrafiltration should launch the suspicion of this complication and the drug should be withdrawn.

The treatment of patients with chronic heart failure and those with asymptomatic left ventricular (LV) dysfunction has focused primarily on patients with LV enlargement and a low ejection fraction (EF). Little attention has been paid to those with a normal chamber size and a low EF. We sought to examine the LV geometry and clinical characteristics in such patients with nondilated cardiomyopathy. Of 3,350 transthoracic echocardiograms performed during a 6-month period, 696 showed an EF of < or =0.45. The patients with an end-diastolic diameter of >56 mm, regional wall motion abnormalities, or valvular disease were excluded. Of the 696 patients, 98 met these criteria, and their medical records were reviewed. The average age was 71 +/- 14 years, and 56% were men. Common co-morbidities included hypertension in 52% and atrial fibrillation (AF) in 43%. Only 22% had disabling cardiac symptoms (functional class III or greater). The average end-diastolic dimension was 49 +/- 5 mm, and the EF was 34 +/- 8%. LV hypertrophic remodeling was present in 53%. A second echocardiogram (422 +/- 177 days after the baseline study) was available for 54 patients. The chamber size was unchanged, but the EF had increased from 33 +/- 8% to 40 +/- 14% (p <0.01). The improvement in EF was seen in the group with AF (33 +/- 6% to 44 +/- 15%, p <0.01) but not in those with normal sinus rhythm (33 +/- 9% to 37 +/- 12%, p = NS). In conclusion, 14% of patients with an EF of < or =0.45 had nondilated cardiomyopathy, often with LV hypertrophic remodeling and/or AF. An improvement in LV function can be expected in many patients with nondilated cardiomyopathy, particularly those with AF., (Copyright 2010 Elsevier Inc. All rights reserved.)

Objectives: This study sought to evaluate the negative predictive value (NPV) of preoperative dobutamine stress echocardiography (DSE) in patients who fail to achieve target heart rate (HR) and assess the influence of resting wall motion abnormalities (WMAs) without demonstrable ischemia on perioperative events., Background: The prognostic value of a negative-submaximal DSE study before noncardiac surgery is unknown., Methods: Consecutive patients (n = 429) who underwent surgery over a three-year period, preceded by DSE, were included. We compared perioperative event rates among those without inducible ischemia according to whether or not 85% age-adjusted maximum HR was achieved, and whether WMAs were present at rest., Results: Of 397 negative DSEs, peak HR was <85% maximum predicted in 62 (16%). Most were receiving beta-blockers (77%). The average dobutamine and atropine doses were 48 microg/kg/min and 1.2 mg, respectively. Average HR was 115 beats/min (74% maximum predicted). Perioperative myocardial infarctions occurred more frequently in patients with positive tests (3 of 32 [9.4%] vs. 7 of 397 [1.8%]; p = 0.03), but with similar frequency among the negative-maximal and negative-submaximal groups (6 of 335, 1.8% vs. 1 of 62, 1.6%, respectively). Accordingly, the NPV was 98% in both subgroups. Events occurred exclusively in patients with WMAs at rest: 7 of 100 (7%) versus 0 of 297 (0%) (p < 0.0001)., Conclusions: In patients undergoing preoperative DSE, failure to achieve target HR is not uncommon despite an aggressive DSE regimen. A negative DSE without resting WMAs has excellent NPV regardless of the HR achieved. Patients with resting WMAs appear to be at increased risk for perioperative events even without provokable ischemia.

We describe a patient with a paradoxical coronary embolism diagnosed by transesophageal echocardiography. The patient developed a stroke followed by a myocardial infarction. Coronary angiography showed an obstruction of the left main coronary artery. Transesophageal echocardiography showed the mechanism of the neurologic and cardiac events to be a paradoxical embolism. Emergency surgical retrieval of the thrombus lodged in the left main coronary ostium and of a separate thrombus traversing a patent foramen ovale was performed. To our knowledge, direct visualization of the paradoxical coronary embolism by echocardiography has not been reported previously. We discuss mechanisms responsible for paradoxical coronary embolism and review the literature pertaining to this condition.

Echocardiographic techniques were used to measure left ventricular isovolumic and ejection phase indexes of contractility in 54 patients with atrial fibrillation, and the relations between cycle lengths and contractility were compared in patients with normal and depressed ejection fractions. Data indicate that variations in contractility occur in a pattern that is consistent with postextrasystolic potentiation and that such interval-dependent potentiation is preserved in patients with atrial fibrillation and depressed ejection fraction.

In 10 patients with atrial fibrillation, echocardiographic measures of left ventricular function-interval relations were used to assess contractility and to test the hypothesis that rhythm regularization produces a higher contractile state than is seen when the rhythm is irregular. Regularization, following direct-current cardioversion, did not augment ventricular contractility above that seen during atrial fibrillation.

In atrial fibrillation (AF), beat-to-beat changes in left ventricular (LV) systolic performance are caused by variations in filling (preload), aortic pressure (afterload), and ventricular inotropic or contractile state. These factors are known to be influenced by the preceding diastolic or RR interval (RR1), but the independent impact of variations in the pre-preceding RR interval (RR2) on contractile state is not well defined. This aspect was studied in 10 patients with lone AF and 8 with coronary artery disease by measuring LV peak ejection velocity (V[pe] Doppler echocardiography) in 80 to 100 consecutive cardiac cycles. V(pe) was plotted against RR1 for beats with a short RR2 and for beats with a long RR2. Such function-interval plots indicate a direct relation between V(pe) and RR1 (for RR1 = 500 to 1,000 ms). In lone AF, the slope (linear fit) of V(pe) versus RR1 was similar for short and long RR2 (slopes = 46 and 50 s[-1]). V(pe), calculated from best linear fit and a common RR1, was consistently higher when RR2 was short than when it was long. At an RR1 = 750 ms, V(pe) (% of max) was 87 +/- 6% when RR2 was short versus 76 +/- 6% when RR2 was long, p <0.05. Results were similar in patients with coronary artery disease and the observed interval-dependent potentiation of contractile state was preserved in patients with a low ejection fraction. By comparing V(pe) at a common RR1, the effects of time-dependent changes in LV preload and afterload are minimized if not abolished. Thus, differences in V(pe) reflect differences in contractile state caused by variations in RR2. Data confirm interval-dependent alterations in contractile state that are likely an expression of the force-frequency relation. Studies of LV function in AF should incorporate a consideration of cycle length-dependent changes in LV contractile state.

Blunt cardiac trauma presents unusual fare for the average cardiologist. The pathogenesis of blunt cardiac injuries is reviewed, and a spectrum of cardiac lesions resulting from blunt trauma is presented, with emphasis on noninvasive diagnostic techniques.

Obstruction of the right ventricular outflow tract from metastatic disease is rare. Eleven previous case reports and three new cases are presented. Two tumor types (pancreas and breast), not previously associated with right ventricular outflow tract obstruction, are included. Congestive symptoms, systolic murmur and right axis deviation or right bundle branch conduction abnormality were universal features. Echocardiography is valuable in the delineation of metastatic cardiac involvement and the detection of intracardiac gradients. Adverse hemodynamic consequences developed in 3 of 10 patients who underwent right heart catheterization in which two died. This procedure should be performed only when absolutely necessary. Metastatic obstruction of the right ventricular outflow tract should be considered in the absence of widespread malignancy because the heart was the sole site of metastasis in 5 of 10 autopsy patients. Two patients with solitary cardiac metastasis benefited from resection of the obstructing tumor, underscoring the importance of early identification of this subgroup.

Four cases are presented in which focal electrocardiographic artifacts mimicked QT segment prolongation with giant T and U waves. Displacement of the recording electrode by a subjacent cardiovascular impulse was the cause of this distortion. The artifacts could be reproduced at the bedside by intentional changes in patient posture and electrode stability. Phasic variation in electrode contact with the electrolyte gel and skin, or intermittent contact between the heart and chest wall, causes shifts in the electrical properties of the recording system which may distort the recorded waveforms during the repolarization phase of the electrocardiogram.

Four patients underwent exercise testing because of a history of pain in the chest; all four developed marked elevation of the S-T segment only during recovery after exercise. Three of the four patients showed ST-segment depression during exercise, but ST-segment elevation was absent until two or more minutes after cessation of exercise. ST-segment elevation after exercise was accompanied by hypotension in three patients and by ventricular arrhythmias in one. Subsequent coronary angiographic studies revealed normal or minimally diseased coronary arteries in two patients and significant coronary lesions in the other two. Review of the literature shows that contrary to the prevailing belief, over half of the patients with Prinzmetal's variant angina have electrocardiographic changes diagnostic of ischemia during exercise testing. Over half of the patients with abnormal findings on tests during exercise display ST-segment elevation as a manifestation of ischemia; however, delayed ST-segment elevation of the type seen in these four patients is distinctly uncommon, having previously been described in only three individual case reports. The pathophysiology of this response is uncertain but may relate to rapid alterations in the autonomic balance during recovery after exercise.

An increase in QRS amplitude with S-T elevation occurs during the acute phase of myocardial infarction, coronary ligation and variant angina. Ischemic conduction delay, postulated as the cause, has not been well characterized. Six patients with transient chest pain, S-T elevation and increase in R-wave voltage also displayed concomitant shift of the frontal QRS axis toward the locus of injury. Electrocardiographic considerations suggest that regional ischemic block, not true hemiblock as has been suggested, offers the most inclusive explanation, providing previously neglected clinical confirmation of experimental observations.

The systemic, pulmonary, and limb circulatory responses to the angiotensin-converting enzyme inhibitor, captopril, were determined in 10 patients with severe, chronic heart failure. Immediate effects include sustained reductions in arterial pressure and pulmonary capillary wedge pressure and improvement in cardiac output, as reported with other vasodilator drugs. Calf vascular resistance did not change despite substantial lowering of total systemic vascular resistance, indicating that arteriolar dilatation occurred on a selective basis. Transient reduction in mean right atrial pressure paralleled slight calf venodilatation, but effects upon the resistance vasculature predominated. Plasma renin activity and norepinephrine concentrations increased after therapy in the acute phase as plasma aldosterone levels consistently fell. During maintenance oral treatment over 7 to 15 months (median, 11.5 months), patients displayed symptomatic benefit, improved functional capacity, and greater exercise tolerance. No major adverse reactions developed. These findings suggest that angiotensin converting enzyme inhibition with captopril in congestive heart failure patients improved cardiocirculatory function through selective arteriolar dilatation. The reordering of regional blood flow which appears to result from release of angiotensin-mediated vasoconstriction, as well as the suppression of aldosterone, may underlie the prolonged benefit observed in these patients. This oral vasodilator appears to represent an effective adjunct for the treatment of advanced, chronic heart failure refractory to conventional measures.

A multicenter randomized double-blind withdrawal study was conducted to compare the efficacy of nifedipine to that of placebo in vasospastic angina. Following a 2-week single-blind nifedipine baseline period, during which nifedipine was maintained at prestudy levels, 38 patients, 19 taking placebo and 19 continuing nifedipine therapy, either completed a 4-week randomized phase or were prematurely withdrawn because of therapeutic failure. During the randomized phase, an increase in median anginal frequency (2.8 attacks/wk, p less than 0.003) and nitroglycerin usage (0.5 tablets/wk, p less than 0.03) occurred only in the placebo group. The randomized phase was prematurely terminated because of anginal exacerbation in 7 of 19 placebo patients (37%) (only 1 patient receiving nifedipine [p = 0.02] experienced anginal exacerbation). Double-blind therapy was judged effective in 16 patients (84%) receiving nifedipine and in 3 patients (16%) receiving placebo (p less than 0.001). Nifedipine was well tolerated. This study establishes the efficacy of nifedipine in the treatment of variant and validates previous clinical experience.

The carotid pulse method of recording systolic time intervals is limited by significant motion-induced artifact, making it unsuitable for studying patients during exercise. As an approach to overcoming this limitation, a new method utilizing the blood velocity profile of the superficial temporal artery measured by Doppler ultrasound has been developed. When compared with the values obtained from the conventional carotid pulse method, Doppler-derived left ventricular ejection time and preejection period showed excellent correlation (r = 0.99 for both) and the Doppler-derived measurements showed little intra- or interobserver variability. Studies performed during treadmill exercise showed that in 8 of 10 subjects, suitable tracing could be recorded through stage 3 of the Bruce protocol, confirming the enhanced stability of the technique compared with the carotid pulse method.

Cigarette smoking is a risk factor for development of coronary atherosclerosis. We examined the relationship between smoking and the anatomic location of coronary artery stenosis in 8,705 patients undergoing cardiac catheterization for suspected coronary artery disease (CAD). The smoking history of patients with CAD (greater than or equal to 70 percent stenosis) was compared with that of control subjects (0 percent stenosis) for each of nine anatomic locations (proximal, middle, and distal segments of right [RCA], anterior descending [LAD], and circumflex arteries [LCX]), using a case-control method. The odds ratio (OR) estimate of relative risk of CAD for smokers relative to nonsmokers was 2.8, with a 95 percent confidence interval (CI) of 2.5 to 3.1. Relative risk was greater for RCA stenosis (OR = 5.8; CI = 4.6-7.2) than for LCX (OR = 3.5; CI = 2.7-4.5) or LAD (OR = 2.1; CI = 1.8-2.4) lesions when comparing smokers with nonsmokers. After control for age, gender, history of diabetes mellitus, and serum cholesterol level, the adjusted relative risk for an RCA lesion (Mantel-Haenszel odds ratio [MOR] = 4.9) was significantly elevated (p less than 0.05) compared with the LAD (MOR = 1.9) but not with the LCX (MOR = 3.1). The relative risks of CAD were the same (p greater than 0.05) for the proximal, middle, and distal coronary segments. Thus, smoking increased the risk of all coronary lesions but did so more for the RCA than for other vessels, suggesting a spatial pattern to the increased risk produced by smoking.

Fifty-two patients underwent coronary artery bypass grafting between 1973 and 1979 for variant angina, defined as pain, usually at rest, associated with S-T segment elevation. Only patients with fixed occlusive coronary artery disease, defined as greater than 70% narrowing in diameter, were included. When fixed coronary artery stenosis is present, variant angina--whether presenting as stable, unstable, or postinfarction angina, and regardless of the number of vessels diseased--is effectively treated by myocardial revascularization. Preoperative intraaortic balloon pumping is a useful therapeutic adjunct in the unstable subset refractory to medical therapy. The results of revascularization in patients with Prinzmetal's variant angina and fixed coronary disease were no different from those in patients with classic angina pectoris of comparable clinical categories.

Gated blood-pool scintigraphy (GBPS) is often obtained as the initial test to evaluate symptoms suggestive of left ventricular dysfunction. Since large pericardial effusions may also cause such symptoms, the ability to recognize them on routine GBPS is of clinical importance. Characteristic features of the "halo" sign surrounding the cardiac blood pool were developed, based on the GBPS of patients with known pericardial effusions. These criteria were then applied blindly to 154 consecutive patients who underwent both GBPS and echocardiography. All five patients with large effusions (approximately greater than 500 ml) were correctly identified by GBPS (sensitivity 100%); for patients with moderate effusions (approximately 150-500 ml), the sensitivity was only 33% (3/9). There were three false positives (specificity 98%). We conclude that large pericardial effusions can be identified with high sensitivity and specificity on routine GBPS. Although echocardiography remains the method of choice for the diagnosis of effusions, inspection for characteristics suggesting their presence on GBPS should be part of routine interpretations.

Thirty-one patients with documented cardiac amyloidosis were compared to 39 control subjects with left ventricular hypertrophy to determine specific 2-dimensional echocardiographic features of amyloid. In 16 patients, increased myocardial echogenicity was present when a single short-axis view was examined, and had a sensitivity of 63% and a specificity of 74% for the diagnosis of amyloidosis. When complete echocardiograms were reviewed (15 patients), an improved sensitivity of 87% and specificity of 81% based on increased echogenicity was seen. Increased atrial septal thickness was present in 60% of amyloid patients and no controls. The combination of increased myocardial echogenicity and increased atrial thickness was 60% sensitive and 100% specific for the diagnosis of amyloidosis. The ratio of electrocardiographic voltage (S in V1 + R in V5 or V6) to left ventricular cross-sectional area also was examined. A ratio of less than 1.5 was 82% sensitive and 83% specific for amyloid (excluding the 2 patients with left bundle branch block), but added little to the diagnosis as determined from the 2-dimensional echocardiogram.

Five patients receiving maintenance hemodialysis for end-stage renal disease underwent therapeutic pericardiocentesis for pericarditis manifested by either cardiac tamponade or effusion unresponsive to conservative therapy. Pericardiocentesis was followed by a one-time instillation of triamcinolone hexacetonide, a nonabsorbable corticosteroid, into the pericardial space with subsequent needle withdrawal. All patients had prompt hemodynamic and symptomatic improvement. Serial echocardiograms showed resolution of the pericardial effusion in all patients. Follow-up evaluation for six months to six years has shown no clinical or postmortem evidence of recurrence. This procedure appears safe and effective and potentially can obviate the need for prolonged catheter drainage or more invasive surgical procedures as therapy for these patients.

A 46 year old patient who presented with an acute myocardial infarction was discovered to have a systemic venous communication with the left heart during attempted insertion of a pulmonary flotation catheter. There was no evidence of cyanosis or systemic arterial desaturation. A right superior vena cava that emptied into the right superior pulmonary vein and a persistent left superior vena cava draining into the coronary sinus were confirmed pathologically after death related to a brain abscess. The embryology, physiology and noninvasive diagnostic approach to this unique venous anomaly are discussed.

To identify the factors that determine operative mortality and long-term survival, we analyzed the data from 3,311 patients who underwent surgical therapy for unstable angina according to clinical presentation. Overall operative mortality was 3.9% and no differences in operative mortality were found between patients with coronary insufficiency, new-onset angina, rest angina, or changing patterns of angina. Logistic regression analysis indicated that age, left ventricular score, and presence of a left main stenosis in a left dominant circulation were related to operative mortality. The 7 year cumulative survival rate was 79%. Features predictive of long-term outcome by Cox analysis included left ventricular score, congestive heart failure score, other illness, extent of coronary disease, and cardiomegaly. Operative mortality of those patients who underwent coronary bypass during their initial hospitalization with unstable angina was similar to that of patients who were discharged and readmitted for operation at a later date. Thus, patients with unstable angina demonstrate a relatively low operative mortality, which is unrelated to the clinical presentation. Long-term survival is primarily determined by clinical and angiographic markers of left ventricular dysfunction, associated illness, and the extent of coronary disease.

Arm exercise assumes an increasingly important role in clinical cardiology as it is used in both exercise testing and training of patients with coronary artery disease. The effects of arm exercise on myocardial oxygen consumption are not well understood; they may differ from the effects of leg exercise. Previous studies have shown that the ischemic threshold is higher in patients performing arm exercise and leg exercise at the same heart rate-blood pressure product. The contribution of other determinants of myocardial oxygen consumption--left ventricular (LV) peak meridional systolic wall stress and contractility--to these observed differences were studied. Thirty healthy subjects exercised to the same peak rate-pressure product during dynamic upper- and lower-extremity exercise. Peak workload was lower during arm exercise (100 +/- 16 W) than during leg exercise (170 +/- 21 W, p less than 0.001). LV wall stress did not differ during either form of exercise (197 +/- 44 vs 204 +/- 33 dynes/cm2 X 10(3), arm vs leg, respectively). This was also true of contractility as assessed by the velocity of circumferential fiber shortening (2.8 +/- 0.6 vs 2.5 +/- 0.4 circ/s, arm vs leg, respectively) and the preejection period/LV ejection time ratio (0.33 +/- 0.11 vs 0.31 +/- 0.07, arm vs leg, respectively). Normal subjects exercising to a similar rate-pressure product showed the same levels of LV wall stress and contractility for arm and leg exercise despite the lower workload performed with arm exercise.

The efficacy of chronic ambulatory captopril (CPT) therapy was evaluated over an 18-month period in 36 patients with refractory chronic congestive heart failure (CHF) by cardiac catheterization, treadmill exercise, nuclear scintigraphy, echocardiography, and symptomatology. Clinical improvement to New York Heart Association functional class I or class II was observed in 63% of the patients (20 of 32) after 2 months of treatment; this amelioration of CHF symptoms was sustained in 63% of the patients (10 of 16) at 18 months. Exercise tolerance increased in 64% of the patients (16 of 25) at early follow-up and in 79% (11 of 14) at late follow-up. Univariate analysis revealed that the pre- and post-CPT stroke work indices (SWI) and the post-CPT cardiac index related to favorable long-term clinical response. Fourteen CHF patients (39%) died during the 18-month follow-up. Univariate analysis revealed that the pretreatment SWI, right atrial pressure, plasma norepinephrine concentration, and echocardiographic shortening fraction were significant predictors of mortality. Multivariate analysis indicated that the SWI was the principal determinant of survival: the 18-month cumulative survival rate for CHF patients with a SWI less than 32 gm . m/m2 was 44% compared to 88% when the SWI was greater than 32 gm . m/m2. Thus, CPT results in sustained symptomatic and functional improvements in patients with advanced CHF, but the mortality remains high and is primarily related to the severity of cardiac dysfunction.