Keith Hickey, M.D.

Thats an easier answer.. You cannot sleep comfortably early after coronary bypass surgery (CABG).. Generally, the first 2 days are in the icu and it is painful. Median sternotomy is essential cutting the sternum in half and closing it back with chicken wire. The surgery team orders out of bed within 14 hours and deep breathing with a pillow on sternum to clear the lungs. Day 3 is transfer day to a Step Down Unit bed. The pain is a little better at this point and patient is starting to walk in the room and sit in the recliner with his inspirometer and cough pillow. At this point, there is some improvement in functional capacity and pain severity with each passing day. By day 5-6, the patient is ready to be discharged to home. Pain levels are still moderate but treatment is effective with short acting opiates ( Oxycodone/hydrocodone) And the patient feels like a human again. The next 2 weeks are about recovering completely. Walking outside some , but not overdoing things. Each day shows incremental improvements. I generally do a follow up visit and tweak the cardiac meds and doses. This visit is short, just to put eyes on my patients. They are still not allowed to drive. Blood pressure usually runs on the low side while the body recovers. The skin staples are removed from the rather long surgical wound, which runs the length of the sternum. The next 4-6 weeks is movement/improvement time. Walking more briskly, and for longer distances. Appetite is better and bodily functions return to previous baselines. This is also the time to start driving short distance and for return to work. Short- term disability forms are completed. Patients are not allowed to lift more than 15 lbs or so. The

Ill pass on this question. Give to someone else. Basically a glass of wine ok anything else I say 6 weeks. But there are no set standards. When Im doubt , dont

Thats an easy answer. There are only 2 diets the ACC and AHA promote. The Mediterranean Diet and the DASH Diet. Both diets have a lot of overlap, but Dash is low sodium for patients with hypertension, CHF, etc. These 2 diets have been shown to improve overall cardiac health, including lowering of both CV morbidity and mortality. This benefit is, in part, due to the reduction of LDL cholesterol and triglycerides. Combined with moderate intensity aerobic exercise for 30 minutes 4-5 times a week, and health benefits improve exponentially. These 2 diets are both low in carbohydrates and saturated fats, with emphasis on olive oil, nuts etc. Warning: it is difficult to be 100% compliant with these diets. They are somewhat bland and not very enjoyable. Realistically, I tell my patients to shoot for a goal of dietary compliance 60-70% of the time. Any more would

Thats a very generalized question. The short answer is yes.. Most arrhythmias originate in the upper chambers of the heart , known as the atria. These arrhythmias are also called supraventricular or above the ventricles. Ventricular arrhythmias originate in either the right or left ventricles. Ventricular arrhythmias are more rare and more dangerous. Arrhythmias that originate in either the right or left atria are not life threatening, with few exceptions. One such situation is when an AV node blocking drug is given to a patient in atrial fibrillation with an underlying electrical bypass pathway ( pre-excitation, such as WPW). The pathway connects the atrium directly to the ventricle, avoiding the physiologic pause in the AV node. The pre-excitation comes from the early depolarization of the ventricle, as the electrical conduction travels through the bypass pathway. This wave is followed shortly after by the slower conduction down the normal pathway of the AV node, bundle of his, and the right and left bundle branches. So the ECG shows a widened QRS with a delta wave, due to the fusion of the double depolarizations of the ventricles superimposed on each other. So if a medication is given that slows the AV node, the conduction down the bypass pathway is unabated. The atrial fibrillation becomes ventricular fibrillation , and cardiac arrest is likely. This is treated by emergent, electrical cardioversion, with successive shocks provided by the automated defibrillator. Ventricular fibrillation requires electrical cardioversion in every case, because it is the ultimate life-threatening arrhythmia. Fibrillation prevents ventricular contractions , and the complete loss of cardiac output, followed by imminent death. Most ventricular arrhythmias are the result of re-entry electrical pathways around scarred ventricular tissue , during or after a myocardial infarction (or heart attack). Antiarrhythmic drugs, such as amiodarone, help maintain sinus rhythm following direct-current cardioversion (shocks). AV nodal blocking agents ( beta-blockers and calcium channel blockers) are largely ineffective, because these arrhythmias originate below the AV node (in the ventricular tissue). There are several varieties of ventricular tachycardia, including inherited channelopathies ( Brugada, Long QT), those related to birth defects causing abnormalities in the ventricles (arrhythmogenic right ventricular dysplasia) , non-compaction syndromes of ventricular tissue , etc. These potentially life threatening arrhythmias are treated with antiarrhythmic drugs and often, implantation of a cardiodefibrillator or AICD. Some of these arrhythmias can be eliminated using ablation therapies by Electrophysiologists. Ablations are certainly a way to avoid long-standing medications. Atrial ,or Supraventricular, arrhythmias come in many forms. Sinus tachycardia is included, but is not considered a true arrhythmia. sinus tachycardia originates in the sinus node and follows the normal electrical conduction pathway. Sinus tach is secondary to increased sympathetic tone from the autonomic nervous system, mediated by the neurotransmitter norepinephrine, or adrenaline. This is triggered by pain, anemia, fever, thyroid hormone, infections etc. The treatment is to correct the underlying cause and slow down the sinus node depolarization and heart rate with the same meds that block the AV node. The true atrial arrhythmias are supraventricular re-entry electrical pathways, ( with or without inclusion of the AV node). Those that do involve the AV node (AVNRT, ectopic atrial tach,or EAT) are converted by maneuvers that increase vagal nerve tone and block the AV node ( valsalva, face submersion in ice water or carotid massage). Also the usual AV blocking meds are effective. The the re-entry arrhythmias that do not involve the AV node (AVRT, WPW), use a bypass pathway as part of the circuit. Since these arrhythmias do not involve the AV node , maneuvers and nodal blocking meds are ineffective. True anti-arrhythmic meds,or electrical shocks, are used to treat these. The most common atrial arrhythmias are atrial fibrillation and atrial flutter. Flutter tends to be unstable long term. Atrial flutter either converts to normal sinus rhythm or degrades into a -fib. The nodal blockers will slow the rates of these tachyarrhythmias, but will not convert them to sinus rhythm. That is done with true anti-arrhythmic drugs ( flecainide, amiodarone, sotalol, dofetillide, dronederone ) and/ or electrical cardioversion. As it pertains to your question, to avoid long term , potentially toxic, anti arrhythmic meds, then the best option is an ablation procedure. The success rate of ablation in AV nodal re-entry tachycardia, or AVNRT, is at 90%. Ablation of bypass pathways , like WPW or AVRT, has about the same efficacy. Ablation of atrial fib is now above 80% , since the pathways of re-entry are around the entry of the pulmonary veins into the left atrium. Ablation of atrial flutter is slightly more effective. the pathway involves the isthmus of the Inferior vena cava and annulus of the tricuspid valve, in the right atrium. In summary, ablation therapy has come a long way in the last decade, with better equipment, better techniques (radio frequency waves vs cryotherapy or freezing the tissue) and less adverse events. To completely avoid long-term medication, ablation procedures are the best option, whether the arrhythmias originate in or above the ventricles. Scar re-entry arrhythmias can usually be ablated, as can some inherited ventricular conduction pathways. However, avoiding long-term medication when treating ventricular arrhythmias might not be an option, regardless of the success of an ablation procedure. The potential for future adverse outcomes can be prohibitive.

It varies depending on the individual .. and how they responded to the new immunosuppressive medications that prevent rejection. In general the post- operative stay in 7 days. Then home bound with mild activity, like walking in the house and short distances outside. After 6 weeks , we recommend cardiac rehab.. rehab is generally 6 weeks. After completing rehab, patients are ready for normal activity and moderate aerobic exercise. In total , about 3 months. As I mentioned, some patients heal quickly and progress independently. Others may take longer, particularly if they have co-morbidities or complications..

The quick and easy answer is dual platelet inhibition to maintain stent patency. The vast majority of stents now are drug eluding DES). The antibiotic /immunotherapy (ie sacrolimus) prevent latent stent stenosis by inhibiting the overgrowth of endothelial tissue from the lining of the artery and late thrombosis . The downside is that with delayed endothelial tissue formation ( stent doesnt become part of the artery lining) exposes the stent scaffolding to clotting factors and platelet activation. This can result in early thrombus/clot in the acute and subacute phase. By using dual platelet blockers that work at different receptors , there is adequate inhibition of platelet aggregation (clumping ) . Platelets are the first line in clotting before the coagulation cascade can be initiated (fibrin). Aspirin works by prostaglandin inhibition (certain prostaglandins promote thrombus ie thromboxane). The PGY2 inhibitors are clopidigrel, prasugrel and ticagrelor. The receptor is another mechanism of stimulating of platelet aggregation. blocking this receptor is more efficacious than the mechanism of aspirin. The treatment with both should be for a year based on our guidelines. 6 months at the least. There is more and more evidence for long term treatment being even better ( 2 years or more). This does increase bleeding risk, particularly in the elderly. So the rusk- benefit Ratio needs to be weighed in each case. The other meds include a statin to prevent recurrence of atherosclerotic plaque in and around the stent ( inhibits plaque development and regressession ) .. also beta-blockers, particularly if the stent was placed for an acute MI (heart attack). The other main class are the ace inhibitors and angiotensin receptor blockers. Particularly in diabetics with heart disease or if there is scarring after the MI with diminished LV function and clinical heart failure. There are other classes of drugs that are used in certain clinical presentations ( aldosterone receptor blockers with significant MI/chf)

At your age brief bradycardia is likely related to the variations in the autonomic nervous system. The influence of the vagal tone. The 10 cranial nerve innervates the organs in the chest and abdomen. The brain can augment heart rate and contractile function of the heart throughout the day. The balance between the sympathetic nervous system, which releases noradrenaline, increases heart rate and contraction of the heart and causes the blood vessels to constrict. Heart rate and blood pressure and cardiac output increase. The parasympathetic nervous system does the opposite. It releases acetylcholine via the vagus nerve and lowers heart rate and dilates the blood vessel and blood pressure drops. They are in balance in most of us ( sympathetic turns organs on during the daily activities and parasympathetic shuts body down at night while sleeping). Dysautonomia is a group of diseases where the brain is signaling the wrong system and symptoms can develop ( syncope, dizzy, palpitations, fast heart rate, etc). The severe cases can get very lightheaded and pass out if standing up too fast. We do a tilt table test to diagnose this disease and treat it with high sodium diets, hydration and certain exercise maneuvers. We especially see this in young , healthy patients with anxiety disorders. The symptoms follow the mood. When the anxiety flares up, they get worse, and vice versa. You are fine. The chances of electrical conductivity disorders in a young healthy patient are very very rare. If that were the case , your heart rate would stay low all the time and cause symptoms. With exercising your heart rate wouldnt increase as necessary and your cardiac output would not be able to sustain the increased workload. You would be fatigued and lightheaded etc. that would require a pacemaker. You dont have and inherent electrical dysfunction and dont need meds or a pacemaker. Check your heart rate with exercise and it should go up to 85% of max (220-age is max). If it doesnt then contact your primary physician. In 20 years of practice Ive never seen a young healthy patient require a pacemaker unless they were born with a congenital electrical heart block. They wouldnt get their heart rate above 40. You are healthy and fine. Quit following your heart rate so closely. Forget about these fluctuations. Sometimes too much technology is not a good thing..

Coronary stents cannot be replaced. The angiographic procedure where stents are deployed in the coronary arteries is called percutaneous intervention or PCI. This would include balloon angioplasty with or without stent placement. There are many nuances to interventions of coronary artery atherosclerotic plaques. The location of plaque (proximal stenosis are more clinically significant), percentage of obstruction of the artery ( >70% required for PCI) bifurcated lesions at side branches, consistency of the plaque (hard, calcified vs softer lipid-rich) length, angular plaque etc. stents we use today are really about 4th generation drug-eluting, to prevent early re-stenosis. PCI, in simplified terms, starts with an angioplasty wire threaded through the portion of the artery still patent. Then a balloon is placed over the wire at lesion location and inflated with a pressure-inflater to smash the plaque against the inner lining of the artery. The stent is then deployed in the same manner to maintain a patent, normal caliber artery. Patient is started on dual anti platelet therapy with low dose aspirin and either plavix, effient or bralinta. After 6 months, the intimal (inner lining of the artery) grows around the stent. The stent becomes part of the artery. So stents are never removed. They couldnt without tearing the artery. However, because the stents change flow patterns in the artery and cause turbulence, new plaque can develop in the stent or at the edges. We then place a new stent inside the previous

Yes. Palpitations are usually due to ectopic beats, either atrial or ventricular. They are usually early after a regular sinus beat, followed by a compensatory pause, as the sinus rhythm resumes before the next sinus node depolarization. Patients can often feel the ectopic beat ( especially premature ventricular contractions, which are more pronounced) or the pause, which feels like a skipped beat. The other possibilities for new palpitations are short runs of sinus tachycardia and/or supraventricular tachycardia (SVT). Tachycardia is abnormally fast heart rates above 100 beats per minute. These heart rate increase are normal in everyone, but not every patient feels the rate changes. The heart rate increases with activity and exercise to elevate cardiac output ( 5-6 liters per minute at rest) to allow the heart to pump extra blood to lower body muscles above resting levels. Most patients feel palpitations at rest, when its quiet. Many patients have underlying stress or anxiety. Ectopic beats, sinus tachycardia and SVT are benign. Only true, sustained and recurring SVT require cardiac consultation to determine the type and treatment options. However, we generally recommend at least a 24 hr holter or Event Monitors to diagnose the exact etiology, to be certain its not runs of atrial fibrillation or atrial flutter. These arrhythmias require more aggressive diagnostic testing and treatment to determine etiology and prevent thromboembolic events ( strokes) from blood clots formed in the left atrium. Rarely, a patient will have a congenital anomaly in the cardiac conduction system resulting in ventricular arrhythmias which are much more serious and occasionally life threatening. However, ventricular arrhythmias are usually confined to patients with underlying damage to the cardiac muscle from heart attacks or other cardiomyopathies (abnormal heart muscle function) from various causes. In a healthy patient with no underlying cardiac diseases, the diagnosis and treatment are routine. the vast majority of patients do fine with low dose beta-blockers, such as long acting metoprolol ( toprol xl), which treat ectopic beats, sinus tachycardia, SVT and symptoms of MVP. Occasionally a a low dose of a safe anti-arrhythmic can be given to otherwise healthy heart patients, like flecainide or propafenone. Generally the causes of ectopic beats ST, SVT can be helped by lifestyle changes ( less caffeine, energy drinks, otc Sudafed containing product, diet pills, and other stimulants ). Treatment of stress, anxiety and dysautonomia may also be necessary.

Answer: this patient is describing atypical chest pain. Not a lot of patient information provide on risk factors for CAD, but age alone goes against true angina from underlying cardiovascular disease. The patient is describing dysphagia with liquids, probably related to esophageal stricture or spasm. True , classic angina is exertional and heaviness or pressure and associated with shortness of breath, nausea, sweating and radiation to jaw or arm(s). Goes away with rest or nitroglycerin. It can be induced with stress and anxiety, and can mimic indigestion. but their is no associated dysphasia. This patient needs gastroenterologist consultation and EGD. If their is a strong family history of CAD, a screening treadmill stress test ,and possibly and echocardiogram , are reasonable plans of action.

DISCUSSION: The likelihood of chest pain representing underlying angina from underlying coronary artery disease, in a 28 yo, is very low. The pain was at rest, with atypical qualities. Classic angina would be described as left sided heaviness or squeezing quality, occurring with exertion, and associated with sweating, shortness of breath, nausea/ vomiting. The pain is usually moderate to severe and can radiate to the neck, jaw or down the left arm/both arms. In this case, the differential diagnoses include esophageal reflux / spasm, costochondritis, pericarditis, pulmonary embolus/infarct (also very low), pleurisy, spontaneous, spontaneous pneumothorax, vasospastic angina (prinzmetals) or coronary dissection. The systems were described as a drink going down wrong to paraphrase. No other associated symptoms were described, such as dyspnea, diaphoresis, nausea or radiation. There was no correlation with exertion, occurring at rest, and no exacerbating or relieving factors. In 20s age range, the differential can be further narrowed down to esophageal spasm, pericarditis, costochondritis/musculoskeletal, pleurisy and coronary spasm/dissection. Pericarditis would be described as sharp and worse with inspiration. That could be ruled out with an ecg (diffuse, upsloping ST segment elevation and PR interval depression) and labs (increased ESR/CRP). Pleurisy would have similar quality, but no abnormalities in the ECG or labs. Spontaneous pneumothorax presents with sharp chest pain and shortness of breath with splinting/shallow, rapid breathing. A standard CXR reveals enlarged, blackened pleural space and compression of the lung on the offending hemi-thorax. Pulmonary emboli are associated with shortness of breath, tachypnea and tachycardia (rapid respiration and heart rate). This patient had no risk factors for deep venous thrombosis/PE, such as surgery/injury/cancer/ immobilization. Coronary vasospasm presents similar to classic angina, and CAD is ruled out with angiography (clean coronaries with no atherosclerotic plaque). ST changes can be noted on the ECG. Pharmacological agents, such as ergonovine , would illicit the spasm narrowing of the coronary artery. Coronary dissection presents similarly, with elevated troponin levels and possible ST depression noted on ECG. CT angiography is the diagnostic test of choice and would show the dissection flap in the offending artery. Both of these entities are less common in this age group and the symptoms described make this unlikely. Which leaves the two most common causes of chest pain in young healthy adults -costochondritis/musculoskeletal and esophageal reflux/spasm. Chondritis is exacerbated by palpating the chest wall and reflux with supine position after meals, particularly spicy foods. GERD is relieved with proton pump inhibitors and chondritis with steroids or NSAIDs.