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Strain


The difference between a strain and a sprain is that a strain involves an injury to a muscle or to the band of tissue that attaches a muscle to a bone, while a sprain injures the bands of tissue that connect two bones together.




strain



Acute strains can be caused by one event, such as using poor body mechanics to lift something heavy. Chronic muscle strains can result from repetitive injuries when you stress a muscle by doing the same motion over and over.


Regular stretching and strengthening exercises for your sport, fitness or work activity, as part of an overall physical conditioning program, can help to minimize your risk of muscle strains. Try to be in shape to play your sport; don't play your sport to get in shape. If you have a physically demanding occupation, regular conditioning can help prevent injuries.


A strain is when a muscle is stretched too much and tears. It is also called a pulled muscle. A strain is a painful injury. It can be caused by an accident, overusing a muscle, or using a muscle in the wrong way.


A strain is an injury to either a muscle or tendon. Tendons are the tough, fibrous bands of tissue that connect muscle to bone. With a back strain, the muscles and tendons that support the spine are twisted, pulled or torn.


Twisting or pulling a muscle or tendon can result in a strain. It can also be caused by a single instance of improper lifting or by overstressing the back muscles. A chronic (long-term) strain usually results from overuse after prolonged, repetitive movement of the muscles and tendons.


The most common complication of a back strain or sprain is a reduction in activity, which can lead to weight gain, loss of bone density, and loss of muscle strength and flexibility in other areas of the body.


This strain of gonorrhea has been previously seen in Asia-Pacific countries and in the United Kingdom, but not in the US. A genetic marker common to these two Massachusetts residents was also previously seen in a case in Nevada, though that strain retained sensitivity to at least one class of antibiotics. Overall, these cases are an important reminder that strains of gonorrhea in the US are becoming less responsive to a limited arsenal of antibiotics.


Gonorrhea has been increasing in Massachusetts and nationally, adding to concerns about the potential spread of this strain which is more difficult to treat. In Massachusetts, laboratory-confirmed cases of gonorrhea have increased 312% since a low point of 1,976 cases in 2009 to 8,133 in 2021. Nationally, confirmed cases have risen by 131% between 2009 and 2021, with 696,764 cases reported in the US in 2021 according to preliminary data released by the CDC.


Segmental strains in apical four-chamber view, showing normal contractions. The color of each trace corresponds to anatomical points on the 2-D color image to the left. The white dotted line represents average strain.


Left panels: left ventricular short-axis view from a healthy individual showing higher radial strains in inner than outer layer. Right panel: Transmural difference in radial strain is a pure geometrical effect, since reduction in external diameter of a passive circular structure leads to more thickening of inner than outer layers. The figure simulates reduction of inner radius by 25% and the numbers indicate the resulting thickening in inner, mid and outer wall layers.11


Left panel: Strain by sonomicrometry in an anaesthetized dog model showing normal contraction in the upper left corner. In the upper right corner, a recording during coronary stenosis showing reduced systolic shortening in combination with marked post-systolic shortening, which implies active contraction and therefore viable myocardium. The two lower recordings illustrate dyskinesia during coronary occlusion. The lower left shows early-systolic lengthening, followed by late and post-systolic shortening, consistent with some degree of active contraction. The lower right recording shows myocardium with no active contraction and reflects the effect of the time-varying left ventricular pressure on the passively behaving myocardium ED = end diastole. Modified from Lyseggen14 and Skulstad.15 Right panel: myocardial strain by tissue Doppler imaging in a patient with acute anterior myocardial infarction. A series of recordings along the septum are displayed. The color of each trace corresponds to anatomical points on the 2-D images to the left. These traces have features similar to the recordings by sonomicrometry in the left panel, illustrating the ability of strain by echocardiography to reflect myocardial segmental contraction Courtsey of Erik Lyseggen.


Left ventricular systolic strain is displayed as bull's eye plot in Figure 4 from a patient with acute myocardial infarction. Suboptimal images with noise artefacts complicate data interpretation and the study can be non-conclusive, but in the majority of patients image quality is satisfactory. This implies, however, that there is some degree of subjectivity in the interpretation of strain images. When the issue is whether a patient has ischaemia, the finding of typical strain features of ischaemia in more than just a single segment favours ischaemic dysfunction rather than noise artefacts. This is illustrated in Figure 5 which shows mild reduction in systolic shortening and post-systolic shortening in several adjacent segments.


An interesting application of GLS is in the evaluation of patients with suspected stable angina pectoris where it was shown to be an independent predictor of significant coronary heart disease, at rest and during dobutamine stress echocardiography.16,17 Another promising application of strain imaging is identification of the relatively large subgroup of non ST-elevation myocardial infarction patients with total coronary occlusion, who needs urgent revascularization.18 Lack of ST elevation in these patients reflects limited sensitivity of electrocardiogram (ECG) in identifying patients with coronary occlusion.19


Post-systolic strain has been proposed as a marker of viability, but should not be used as a stand-alone index since post-systolic shortening also occurs also in myocardium with transmural necrosis or scar (Figure 6). In the latter case, there is typically systolic lengthening, and post-systolic shortening is due to passive recoil when LV pressure is falling during isovolumic relaxation. Furthermore, load-dependent interactions with non-ischaemic myocardium can modify systolic strain.20,21 When there is systolic hypokinesia or akinesia indicating some degree of active contraction, post-systolic shortening is attributed to active contraction and reflects viable myocardium.14 Importantly, a segment which is entirely passive during the first few hours after coronary occlusion, may yet not be irreversibly injured and may recover with reperfusion.15 In the chronic phase after an infarct, however, an entirely passive strain curve is most likely a sign of scarring. There are limited clinical data to verify these concepts which have been well documented in experimental models.


Longitudinal strain by speckle-tracking echocardiography (two-chamber view) in a patient with acute myocardial infarction the day after percutaneous coronary intervention of an occluded left anterior descending coronary artery. Follow-up late enhancement cardiac magnetic resonance (lower left) showed myocardial scarring represented by the white area in apex and anterior wall. Strain curves display typical features of ischaemic dysfunction, ranging from lengthening throughout systole in a segment with transmural infarction and different degrees of dysfunction in other segments. The color of each trace corresponds to anatomical points on the 2-D color image and the white dotted line shows the average of the six strain curves. The yellow curve shows normal contraction in a non-infarcted segment.


Prognosis in HCM is closely related to LV function and morphology.28 In contrast to LVEF which very often is normal in HCM, longitudinal strains are reduced in early stages of the disease, whereas radial and circumferential strains may be preserved (Figure 7). Longitudinal strain is reduced at the site of hypertrophy, commonly in the interventricular septum. Current clinical practice guidelines for management of HCM29 include strain echocardiography for evaluating longitudinal function in early disease. Longitudinal function can be abnormal even before development of increased wall thickness in mutation positive family members29 (Figure 7). The finding of reduced longitudinal strain, particularly in the presence of an abnormal ECG, increases the probability of disease.


Longitudinal strain curves from apical four-chamber view in a 28-year-old male who was positive for a hypertrophic cardiomyopathy-related mutation in the MYBPC3 gene detected by family genetic screening. The color of each trace corresponds to anatomical points on the 2-D color image to the left. Average strain from four-chamber view was 14% (white dotted trace) and global longitudinal strain was 16%, indicating reduced longitudinal function. Ejection fraction was 57%. He was asymptomatic and had no hypertrophy by echocardiography, cardiac magnetic resonance nor by electrocardiography. Green vertical line indicates timing of AVC.


The diagnosis of pathological hypertrophy in young healthy athletes is challenging and preliminary data suggest that strain imaging may be of help as reduction in systolic strain, which is typical for HCM, is not found in physiological hypertrophy.30 Further validation is needed, however, before this application of strain imaging can be recommended as routine. Of the echocardiographic parameters, the single most important discriminator is LV end-diastolic diameter since hypertrophy in HCM occurs at the expense of cavity size, resulting in a small LV cavity (


Arrhythmogenic right ventricular cardiomyopathy (ARVC) is diagnosed according to the 2010 Task Force Criteria33 using different modalities including imaging by echocardiography and cardiac magnetic resonance (CMR). Reduced RV function by reduced RV-free wall strain and a dyssynchronous RV contraction pattern have been shown to be early markers of ARVC,34,35 and may help diagnosis in early phases of disease. 041b061a72


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