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Do you want more traffic from Google, without creating new content or acquiring new backlinks? Then you should optimize for featured snippets.

If you’re wondering what featured snippets are, here’s an example:

Basically, it’s when Google shows an answer, or a partial answer to the question directly in the search results.

You’ve probably seen these before; they tend to pop upfor a lot of “informational” searches(such as questions). In fact, According to buy cheap official outlet new styles Gadea Womens 40659 Oxford Shoes Multicolour Sweet Stone / Atenea Canela outlet best prices real sale online v4ss7
, Google shows featured snippets for ~12.3% of search queries, which is a lot.

But before I show you how to easily find and steal featured snippets—and secure the ones you already own—you may be wondering:

I f answers to queries are displayed directly in the SERPs (by featured snippets), won’t this mean that fewer people tend to click on search results, effectively driving less traffic to my website?”

Let me answer that for you!

For SERPs wi th featured snippets, 8.6% of all clicks go to the featured snippet on average (according to our study).

This means that featured snippets effectively steal traffic away from the other organic results, including the result in position #1.

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of 2 million featured snippets.

But what does this mean in real terms?

What does this mean if I already rank in position #1?“

If you rank in position #1 AND ownthe featured snippet, 28.2% of all clicks will go to your page . (That’s clicks to the featured snippet and the regular #1 result combined.)

28.2% of all clicks will go to your page

If you rank #1 and DO NOT ownthe featured snippet (but a competitor does): only 19.6% of all clicks will go to your page .

19.6% of all clicks will go to your page

That’s means you get ~31% LESS traffic by NOT owning the featured snippet.

Table 39 lists the pharmacological components of OMT. For practical purposes the mnemonic ‘ABCDE’ approach has been proposed: ‘A’ for antiplatelet therapy ( Table 36 ), anticoagulation, angiotensin-converting enzyme inhibition, or angiotensin receptor blockade; ‘β’ for β-blockade and blood pressure control; ‘C’ for cholesterol treatment and cigarette smoking cessation; ‘D’ for diabetes management and diet; and ‘E’ for exercise.

Table 39
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Long-term medical therapy after myocardial revascularization

Table 39
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Long-term medical therapy after myocardial revascularization

Table 36
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Antithrombotic treatment options in myocardial revascularization

Table 36
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Antithrombotic treatment options in myocardial revascularization

Cardiac rehabilitation and secondary prevention programmes are implemented in or out of hospital, according to the clinical status and the local facilities. A structured in-hospital (residential) cardiac rehabilitation programme, either in a hospital or in a dedicated centre, is ideal for high-risk patients, who may have persistent clinical, haemodynamic, or arrhythmic instability, or severe complications or comorbidities.

After uncomplicated PCI or CABG procedures, physical activity counselling can start the following day, and such patients can walk on the flat and up the stairs within a few days. After a revascularization procedure in patients with significant myocardial damage, physical rehabilitation should start after clinical stabilization.

The following general criteria should be considered in planning an exercise testing modality for exercise prescription: safety, i.e. stability of clinical, haemodynamic, and rhythmic parameters, ischaemic and angina threshold (in the case of incomplete revascularization), degree of LV impairment; associated factors (i.e. sedentary habits, orthopaedic limitations, occupational and recreational needs).

Although the need to detect restenosis has diminished in the DES era, a sizeable proportion of patients are still treated with BMS or balloon angioplasty with high recurrence rates. Likewise, the durability of CABG results has increased with the use of arterial grafts and ischaemia stems mainly from SVG attrition and/or progression of CAD in native vessels.

Follow-up strategies should focus not only on the detection of restenosis or graft occlusion, but also on the assessment of patients’ functional status and symptoms, as well as on secondary prevention. A baseline assessment of physical capacity is needed when entering a rehabilitation programme after revascularization [ 265 ].

Both epicardial and endocardial tissues in hearts with healed infarcts demonstrate marked disparity in refractoriness in the border and infarct areas, especially during sympathetic stimulation [27] . The prolongation of refractoriness could be related to a slowed recovery of I Na or delay in deactivation of outward K + currents in the infarct substrate. To date however, there have been no direct measurements of these latter currents in cells overlying the healed infarct.

In rabbit 8 weeks post MI, it appears that the abnormally prolonged APs are accompanied by not only a reduction in L type Ca 2+ current activity (see above) but also an increase in NaCa exchanger current density (normal mode) [14] . Again it is not known whether NaCa exchanger kinetics are altered in these myocytes from the healed infarct hearts.

Structural remodeling of the left ventricle after myocardial infarction involves the regions of necrosis and infarct scar, the central and border zone areas as described above (substrate), as well as the noninfarcted myocardium remote from the arrhythmic infarct substrate. In many models, the noninfarcted myocardium shows gradual morphological changes indicative of hypertrophy as it adapts to the increased workload of the compromised heart both during the subacute or healing (3 days, weeks) or chronic, healed (2-month) stages.

Regional hypertrophy that accompanies ventricular remodeling is of interest since left ventricular hypertrophy is a strong risk factor for ventricular arrhythmias [51] . Remote areas include noninfarcted LV or RV tissue. Large (40% of LV) infarcts tend to show greater increases in cell size in the non-infarcted remote areas, compared to smaller infarcts (<15%) [52] . Non-transmural infarcts show increases in cell diameter adjacent to the infarct, but not in the remote areas; conversely, in transmural infarcts, all cell diameters increase [52] . In some experimental models increases in myocyte length but not width have been described [15] .

I K1 is reduced in epicardial but not endocardial LV myocytes of 3-day-old rat infarcted heart. Minor changes in I K1 density occur in RV myocytes remote from the infarcted region of the 3 day rat heart [53] . It is unlikely that these changes would be accompanied by a change in resting potential of the myocytes. No change in resting potential is seen in myocytes dispersed from the 3-week infarcted rat heart [54] .

Differences in AP amplitude, and V̇ max between post-MI and sham cells, both those from the endocardial and epicardial regions are related to the type of MI model studied. V̇ max of epicardial cells is lower than that of endocardial cells in the post-MI remodeled LV [54] .

Hypertrophied LV myocytes remote from a 3 week MI scar show a significant increase in I CaL amplitude but when normalized to cell capacitance changes, no significant change in I CaL density is observed [54] . A reemergence of the T type Ca 2+ current has been reported to occur in myocytes of the hypertrophied rat ventricles [55] .

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