Both chronic microgravity exposure and long-duration bed rest induce cardiac atrophy, which leads to reduced standing stroke volume and orthostatic intolerance. However, despite the fact that women appear to be more susceptible to postspaceflight presyncope and orthostatic hypotension than male astronauts, most previous high-resolution studies of cardiac morphology following microgravity have been performed only in men. Because female athletes have less physiological hypertrophy than male athletes, we reasoned that they also might have altered physiological cardiac atrophy after bed rest. Magnetic resonance imaging was performed in 24 healthy young women (32.1 +/- 4 yr) to measure left ventricular (LV) and right ventricular (RV) mass, volumes, and morphology accurately before and after 60 days of 6 degrees head-down tilt (HDT) bed rest. Subjects were matched and then randomly assigned to sedentary bed rest (controls, n = 8) or two treatment groups consisting of 1) exercise training using supine treadmill running within lower body negative pressure plus resistive training (n = 8), or 2) protein (0.45 g x kg(-1) x day(-1) increase) plus branched-chain amino acid (BCAA) (7.2 g/day) supplementation (n = 8). After sedentary bed rest without nutritional supplementation, there were significant reductions in LV (96 +/- 26 to 77 +/- 25 ml; P = 0.03) and RV volumes (104 +/- 33 to 86 +/- 25 ml; P = 0.02), LV (2.2 +/- 0.2 to 2.0 +/- 0.2 g/kg; P = 0.003) and RV masses (0.8 +/- 0.1 to 0.6 +/- 0.1 g/kg; P < 0.001), and the length of the major axis of the LV (90 +/- 6 to 84 +/- 7 mm. P < 0.001), similar to what has been observed previously in men (8.0%; Perhonen MA, Franco F, Lane LD, Buckey JC, Blomqvist Zerwekh JE, Peshock RM, Weatherall PT, Levine BD. J Appl Physiol 91: 645-653, 2001). In contrast, there were no significant reductions in LV or RV volumes in the exercise-trained group, and the length of the major axis was preserved. Moreover, there were significant increases in LV (1.9 +/- 0.4 to 2.3 +/- 0.3 g/kg; P < 0.001) and RV masses (0.7 +/- 0.1 to 0.8 +/- 0.2 g/kg; P = 0.002), as well as mean wall thickness (9 +/- 2 to 11 +/- 1 mm; P = 0.02). The interaction between sedentary and exercise LV and RV masses was highly significant (P < 0.0001). Protein and BCAA supplementation led to an intermediate phenotype with no change in LV or RV mass after bed rest, but there remained a significant reduction in LV volume (103 +/- 14 to 80 +/- 16 ml; P = 0.02) and major-axis length (91 +/- 5 to 88 +/- 7 mm; P = 0.003). All subjects lost an equivalent amount of body mass (3.4 +/- 0.2 kg control; 3.1 +/- 0.04 kg exercise; 2.8 +/- 0.1 kg protein). Cardiac atrophy occurs in women similar to men following sedentary 60 days HDT bed rest. However, exercise training and, to a lesser extent, protein supplementation may be potential countermeasures to the cardiac atrophy associated with chronic unloading conditions such as in spaceflight and prolonged bed rest.
Takotsubo cardiomyopathy (TC) is characterized by transient, often severe, left ventricular dysfunction and electrocardiographic changes that might mimic acute myocardial infarction in the absence of significant obstructive coronary artery disease. It is often encountered in elderly women after physical or emotional stress. Excessive catecholamine stimulation, metabolic abnormalities, and microcirculatory dysfunction are thought to be responsible for the manifestations of this disorder. This comprehensive review summarizes relevant published data, atypical presentations, pathophysiology, and management strategy. It also includes a review of 789 patients with TC including nine illustrative cases encountered at our institution.
Antianginal and lipid-lowering medications may modify the results of stress myocardial perfusion imaging. Several studies have shown the beneficial potential of these agents in suppressing myocardial ischemia in patients with known coronary artery disease. The effects of nitrates, calcium-channel blockers, beta-blockers, and statins on myocardial perfusion imaging are likely attributable to changes in myocardial blood flow and myocardial oxygen supply-demand ratio. This comprehensive review examines relevant experimental and clinical published data. Technical issues in image interpretation specific to myocardial perfusion imaging and implications of use of cardiac medications to results of myocardial perfusion imaging are discussed.
Both chronic microgravity exposure and long‐duration bed rest induce cardiac atrophy, which leads to reduced standing stroke volume and orthostatic intolerance. However, despite the fact that women appear to be more susceptible to post‐spaceflight presyncope and orthostatic hypotension than male astronauts, most previous high‐resolution studies of cardiac morphology following microgravity have been performed only in men. Because female athletes have less physiological hypertrophy than male athletes, we reasoned that they also might have altered physiological cardiac atrophy after bed rest. Magnetic resonance imaging was performed in 24 healthy young women (32.1±4 years) to measure left ventricular (LV) and right ventricular (RV) mass, volumes, and morphology accurately before and after 60 days of 6° head‐down tilt (HDT) bed rest. Subjects were matched and then randomly assigned to sedentary bed rest (controls, n=8) or two treatment groups consisting of (1) exercise training using supine treadmill running within lower body negative pressure plus resistive training (n=8), or (2) protein (0.45 g/kg/day increase) plus branched‐chain amino acid (BCAA) (7.2 g/day) supplementation (n=8). After sedentary bed rest without nutritional supplementation, there were significant reductions in LV (96±26–77±25 mL; P=0.03) and RV volumes (104±33–86±25 mL; P=0.02), LV (2.2±0.2–2.0±0.2 g/kg; P=0.003) and RV masses (0.8±0.1–0.6±0.1 g/kg; P<0.001), and the length of the major axis of the LV (90±6–84±7 mm. P<0.001), similar to what has been observed previously in men (8.0%; Perhonen M.A., Franco F., Lane L.D., Buckey J.C., Blomqvist Zerwekh J.E., Peshock R.M., Weatherall P.T., Levine B.D. J Appl Physiol 2001: 91: 645–653). In contrast, there were no significant reductions in LV or RV volumes in the exercise‐trained group, and the length of the major axis was preserved. Moreover, there were significant increases in LV (1.9±0.4–2.3±0.3 g/kg; P<0.001) and RV masses (0.7±0.1–0.8±0.2 g/kg; P=0.002), as well as mean wall thickness (9±2–11±1 mm; P=0.02). The interaction between sedentary and exercise LV and RV masses was highly significant (P<0.0001). Protein and BCAA supplementation led to an intermediate phenotype with no change in LV or RV mass after bed rest, but there remained a significant reduction in LV volume (103±14–80±16 mL; P=0.02) and major‐axis length (91±5–88±7 mm; P=0.003). All subjects lost an equivalent amount of body mass (3.4±0.2 kg control; 3.1±0.04 kg exercise; 2.8±0.1 kg protein). Cardiac atrophy occurs in women similar to men following sedentary 60 days HDT bed rest. However, exercise training and, to a lesser extent, protein supplementation may be potential countermeasures to the cardiac atrophy associated with chronic unloading conditions such as in spaceflight and prolonged bed rest.
Tako-tsubo cardiomyopathy (TC) typically presents with chest pain, ST changes, and transient left ventricular (LV) apical ballooning in the absence of epicardial coronary artery disease (CAD). This process is reversible and usually benign. An unusual manifestation is that of left ventricular outflow tract (LVOT) obstruction with systolic anterior motion of the mitral valve. Recognition of this finding is critical in patient management especially in the setting of cardiogenic shock, as inotropes are likely to aggravate and worsen the clinical condition. We provide a systematic review and an illustrative case, and discuss treatment strategies.Key words: tako-tsubo cardiomyopathy, left ventricular outflow tract obstruction, coronary vasospasm, left ventricular apical ballooning Tako-tsubo cardiomyopathy (TC) mimics acute myocardial infarction (MI) and should be considered in all patients, especially post-menopausal women who present with transient left ventricular (LV) dysfunction in the absence of obstructive coronary artery disease (CAD). Approximately 2% of all patients presenting with a presumed diagnosis of ST segment elevation MI have this syndrome, 1 and 87% of the reported cases of TC are post-menopausal women with a mean age of 68. 2 While TC frequently presents with substernal chest pain, these patients might present with electrocardiogram (ECG) changes alone, shortness of breath, or cardiogenic shock. 3 The ECG changes include ST elevation, ST depression, Twave inversion, pathologic Q waves, and QT prolongation. New left and right bundle branch blocks have been reported, 4 but the most common ECG changes are ST elevation (68%), which is most commonly seen in the precordial leads and diffuse T-wave inversions (97%). 2,4 The frequency of ST depression and Q waves is ∼10% and 27%, respectively. 3 -5 There is usually mild elevation of troponin, and less commonly, creatine kinase (CK) and its isoenzyme CK-MB, but the pattern differs from that seen following MI. In fact, cardiac enzyme levels peak at the onset of symptoms, and they do not slowly rise and fall as in MI.2,4 Troponin and CK-MB levels are elevated in 86% and 74% of the cases, respectively. 6Several LV wall motion abnormalities have been described in the setting of TC. The classic abnormality involves ballooning of the distal LV segments and apex as a result of severe hypokinesia, akinesia, or dyskinesia. At the same time, there is compensatory basal hyperkinesia. A less common variant involving mid-LV dyskinesia has also been described. 7 These transient LV wall motion abnormalities can be detected by left ventriculography, 2-Dimensional echocardiography (2DE), gated single photon emission computed tomography (SPECT), and magnetic resonance imaging (MRI), and usually involve multiple vascular territories. 8 The pathophysiology behind TC is poorly understood. However, according to a recent large systematic review of 542 cases, physical or emotional stress precipitated the reversible LV dysfunction in ∼80% of the cases. 2Excessive sympathetic stim...
Bed rest deconditioning leads to physiological cardiac atrophy, which may compromise left ventricular (LV) filling during orthostatic stress by reducing diastolic untwisting and suction. To test this hypothesis, myocardial-tagged magnetic resonance imaging (MRI) was performed, and maximal untwisting rates of the endocardium, midwall, and epicardium were calculated by Harmonic Phase Analysis (HARP) before and after -6 degrees head-down tilt bed rest for 18 days with (n = 14) and without exercise training (n = 10). LV mass and LV end-diastolic volume were measured using cine MRI. Exercise subjects cycled on a supine ergometer for 30 min, three times per day at 75% maximal heart rate (HR). After sedentary bed rest, there was a significant reduction in maximal untwisting rates of the midwall (-46.8 +/- 14.3 to -35.4 +/- 12.4 degrees /s; P = 0.04) where untwisting is most reliably measured, and to a lesser degree of certainty in the endocardium (-50.3 +/- 13.8 to -40.1 +/- 18.5 degrees /s; P = 0.09); the epicardium was unchanged. In contrast, when exercise was performed in bed, untwisting rates were enhanced at the endocardium (-48.4 +/- 20.8 to -72.3 +/- 22.3 degrees /ms; P = 0.05) and midwall (-39.2 +/- 12.2 to -59.0 +/- 19.6 degrees /s; P = 0.03). The differential response was significant between groups at the endocardium (interaction P = 0.02) and the midwall (interaction P = 0.004). LV mass decreased in the sedentary group (156.4 +/- 30.3 to 149.5 +/- 27.9 g; P = 0.07), but it increased slightly in the exercise-trained subjects (156.4 +/- 34.3 to 162.3 +/- 40.5 g; P = 0.16); (interaction P = 0.03). We conclude that diastolic untwisting is impaired following sedentary bed rest. However, exercise training in bed can prevent the physiological cardiac remodeling associated with bed rest and preserve or even enhance diastolic suction.
The diagnosis of Takotsubo cardiomyopathy (TC) must be considered in all patients who develop transient left ventricular apical (or mid ventricular) ballooning in the absence of obstructive coronary artery disease (CAD). Although the prevalence of TC remains unknown, approximately 2% of all patients presenting with a presumed diagnosis of ST elevation myocardial infarction have been found to have this syndrome. TC usually occurs in the setting of physical or emotional stress associated with excessive sympathetic stimulation and catecholamine release. A literature review and illustrative case report are provided.
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