Monthly Archives: May 2014

Percutaneous ventricular restoration therapy

Percutaneous ventricular restoration therapy

This is a new form of device therapy for heart failure. The device used is Parachute implant® (http://www.cardiokinetix.com/).

Parachute implant is an umbrella shaped device that is inserted into the left ventricle.

Pathophysiological basis of use:

–          In post MI patients there is progressive LV remodelling (progressive dilatation of the               left ventricle).

–          This dilatation of the ventricle increases the LV wall stress.

wall stress = (LV pressure  × LV diameter)÷  ( 2×LV wall thickness )

–          Increased LV wall stress increases LV afterload

–          Increased LV afterload worsens the LV dysfunction.

What the device does:

This device is useful in patients with old anterior and antero-apical infarctions and LV             dysfunction.

–          Parachute implant separates the dilated apical portion of the left ventricle from the                 normally contracting LV.

–          There by improves the LV geometry

–          Reduces the LV afterload

–          Improves LV function

Data regarding efficacy:

In a recent study presented at ESC heart failure congress,

–          There was a significant reduction in LV end-diastolic (120.8 vs 103.8) an end-systolic volumes (87.6 vs 73.2) at 12 months after parachute implant. There was significant increase in LVEF (28.4 vs 30.4).

–          Symptomatic improvement

–          Improvement in functional class

–          It might improve heart failure related admissions and mortality.

Risks:

–          Interference of the device with papillary muscles or apical chordae tendineae is unknown

–          Risks and consequences of dislocation.

–          Thrombo-embolic risk.

Ongoing Trials:

PARACHUTE IV

 Conclusion:

This device represents a percutaneous alternative for LV reduction surgeries. Long term safety and efficacy results to be seen.

APPOSITION IV : Trial

STENTYS SELF APPOSITION SES:

It is a self-expandable sirolimus-eluting coronary stent system, similar in concept to other self-expanding systems.

Watch the video:

Stentys self-apposition SES

APPOSITION IV trial:

Patients – 152 patients presenting with STEMI.

Design: Patients were randomized to Stentys self-apposing SES (Stentys, Paris, France; n = 90)   vs Resolute zotarolimus-eluting stent (ZES; Medtronic, Santa Rosa, CA; n = 62). Each treatment arm was then randomized to either 4- or 9-month follow-up.

 -Results: On QCA, no differences were observed between the treatment arms just after the procedure for in-stent minimal and mean lumen diameter. In-stent mean lumen diameter was larger at both 4- and 9-month follow-up for Stentys compared with Resolute (3.39 ± 0.46 mm vs 3.13 ± 0.35 mm).

-OCT demonstrated that Stentys SES was associated with fewer malapposed struts (0.07 ± 0.26% vs 1.16 ± 1.59%) and more covered struts (94.32 ± 5.69% vs 89.09± 5.65%) than Resolute ZES at 4 months. Percentage of stents with all struts covered was also higher with Stentys compared to Resolute ZES (33.3% vs 3.8%).

-No differences in malapposition (P = .55) or coverage (P = .81) were seen between the treatment arms in the 9-month cohort.

-Clinical outcomes were low and well balanced between stent groups in terms of MACE (P = .46), TVF (P = .46), and target vessel MI (P = .39).

-Predilatation Needed.

-The device is larger in profile as compared to DES

 Conclusion: Stentys, a self-apposing sirolimus-eluting stent (SES), shows ‘excellent’ apposition over time—better than an existing balloon-expandable drug-eluting stent—in patients with ST-segment elevation myocardial infarction (STEMI). The newer device is associated with faster strut coverage.

Your comments and insight most welcome

 

Coronary artery disease

Coronary artery disease

The heart like any other organ in the body needs constant supply of blood to survive. Blood reaches different parts of the heart through the coronary arteries.  Coronary arteries are of vital importance for the sustenance of life.

The different  normal functions of the coronary arteries include:

1. Carrying blood to different  parts of the heart

2. Regulating  blood supply to the heart in the face of varying blood pressure

3. Increasing blood supply to the heart in the face of increased cardiac demand like during exercise.

The coronary arterial system:  Can be divided into four parts

1. Left main coronary artery (LMCA)

        Which divides into

2. Left anterior descending artery  (LAD) And

3. Left circumflex artery (LCX)

4. Right coronary artery (RCA)

LMCA

Left main coronary artery, left anterior descending and left circumflex coronary artery

RCA

Right coronary artery

What is coronary artery disease (CAD)

Any disease which involves coronary arteries is CAD. Usually the most common form is reduction in the size of the coronary arteries. Many disease conditions can result in coronary artery disease but the most common cause of CAD is atherosclerosis. Other diseases like autoimmune diseases, congenital diseases can result in CAD.

Why CAD occurs?

CAD occurs due to a variety of reasons, which are called risk factors. You can read more about risk factors here.

What are the types of CAD?

CAD is a septum of diseases and it is divided to two categories

1. Chronic stable angina (CSA): In CSA there is a pattern of chest discomfort associated with exertion or emotional excitability. The occurrence of angina is after a predictable amount of work.

2. Acute coronary syndromes ( ACS)

ACS are are again divided into three types

A. Unstable angina: When there is new onset angina, worsening of previous angina, rest angina, it is called unstable angina

B. Non-ST elevation myocardial infarction

C. ST elevation myocardial infarction – the classic heart attack

This classification is important for the point of view of management and the aggressiveness of treatment.

What are the symptoms of coronary artery disease?

 A. Angina : Chest pain or discomfort .

B. Angina equivalents – fatigue , dyspnoea (shortness of breath) , eructations, palpitation

C. Sudden onset acute severe chest pain

D. Cold sweating

Read more about symptoms of heart disease here.

What to do?

First of all see your doctor for evaluation and treatment. Some of the general management modalities are discussed here.

Investigations

For the diagnosis of CAD the following investigations may be needed:

A. ECG – is of central importance in CAD. ECG in many occasions shows changes suggestive of reduced myocardial blood flow

B. Stress test – Different types of stress tests are available like treadmill test, nuclear stress  tests. A stress test can be done by performing exercise on a treadmill or by giving drugs in patients who are unable to do exercise. It is done when the symptoms are not typical and ECG changes are not typical.

C. Echocardiography – is for assessment of structure and function of heart

D. CT coronary angiography – It  is a noninvasive imaging modality for the diagnosis of CAD. It is like any other CT scan. Contrast injections are given to visualize the coronary arteries

E. MRI coronary angiography – Not very widely used for imaging of coronary arteries

F. Coronary angiography – this is the gold standard for the diagnosis of coronary artery disease and any percutaneous treatment for CAD can be done in the same setting

Treatment:

A. Risk factor control – Risk factor control is one of the most effective interventions for reducing the impact of coronary heart disease.  Proper control of blood pressure, diabetes, quitting smoking, treatment of abnormalities of cholesterol are some of the steps that greatly reduce the incidence and prevalence of CAD.

B. Medications- Patients with CAD will on some medications indefinitely (usually life long). For chronic stable angina, the first line of treatment is usually medical management. Even  patients who undergo coronary artery stenting or bypass surgery need to take medicines life long.

C. Coronary angiography and percutaneous coronary interventions are usually advised for patients who have more serious symptoms or for whom symptoms are not easily controlled with medicines. In presence of certain high risk factors patients should undergo early angiography and intervention or surgery

D. Coronary artery bypass grafting (CABG)

Drugs used in treatment of CAD:

1. Anti- platelets e.g. Aspirin, Clopidogrel, Prasugrel, ticagrelor, etc

2. Statins e.g. rosuvastatin, atorvastatin etc

C. Beta blockers (metoprolol, bisoprolol etc)

D. Ace inhibitors or angiotensin receptor blockers

E. Anticoagulants (heparin)

F. Nitrates

G. Nikorandil

H. Ranolazine

I. Trimetazadine

H. Therapies for refractory angina

Details about each class of drug I will post each week( Monday )

So please follow up

Cardiac interventions for CAD:

Known as percutaneous coronary intervention(PCI). In this procedure coronary angiography is done and then stenting is done as required.

Coronary artery bypass grafting:

CABG may be needed where PCI is not feasible or doesn’t give optimum results.

Finally there are a spectrum of patients who have drug refractory angina who are not suitable for PCI or CABG. They have refractory angina and the treatment options are limited in such patients.

Conclusion: Coronary artery disease is the leading cause of death and suffering in the world. The most common symptoms include chest pain, shortness of breath. It is diagnosed by ECG, stress tests, coronary angiography etc. The treatment include risk factor reduction, medical management and PCI or bypass surgery as needed.

Key words: Patient information, Coronary artery disease, heart disease, coronary angiography, ECG, Angina, CAD, PCI, CABG

Vorapaxar (Zontivity) approved

CardioSource – FDA Approves Vorapaxar to Reduce Heart Attack and Stroke Risks in HighRisk Patients.

The U.S. Food and Drug Administration (FDA) has approved vorapaxar (Zontivity) to reduce the risk for MI, stroke, cardiovascular-related death and coronary revascularization among patients who have previously experienced MI or peripheral artery disease.

Vorapaxar is the first in a new class protease-activated receptor-1 (PAR-1) antagonist drugs

targets thrombin-induced platelet activation.

In patients who have had a heart attack or who have peripheral arterial disease, this drug will lower the risk of heart attack, stroke, and cardiovascular death.

In the study that supported the drug’s approval, Zontivity lowered this risk from 9.5 percent to 7.9 percent over a 3-year period – about 0.5 percent per year.

Adverse effects include excess bleeding and easy bruisability

A 2011 clinical trial (TRA 2P-TIMI 50 Presentation Slides (Morrow))showed vorapraxar, added to other anti-platelet agents (generally aspirin and clopidogrel), reduced the rate of a combined endpoint of heart attack, stroke, cardiovascular death, and coronary revascularization when compared to placebo.

Genetic mutation in Metabolic Syndrome

A Form of the Metabolic Syndrome Associated with Mutations in DYRK1B — NEJM.

 

A founder mutation was identified in DYRK1B, substituting cysteine for arginine at position 102 in the highly conserved kinase-like domain. The mutation precisely cosegregated with the clinical syndrome. Functional characterization of the disease gene revealed that nonmutant protein encoded by DYRK1B inhibits the SHH (sonic hedgehog) and Wnt signaling pathways and consequently enhances adipogenesis. Furthermore, DYRK1B promoted the expression of the key gluconeogenic enzyme glucose-6-phosphatase. The R102C allele showed gain-of-function activities by potentiating these effects. A second mutation, substituting proline for histidine 90, was found to cosegregate with a similar clinical syndrome in an ethnically distinct family.

Conclusions

These findings indicate a role for DYRK1B in adipogenesis and glucose homeostasis and associate its altered function with an inherited form of the metabolic syndrome.

APPROACH TO SYNCOPE

APPROACH TO SYNCOPE
History taking in cardiology cont.
Syncope has been defined by the European society of cardiology as “A transient loss of consciousness due to transient global cerebral hypoperfusion characterized by rapid onset, short duration, and spontaneous recovery.”
Syncope is a common problem, it causes significant agony and apprehension and may result in serious injury to the patient. Analysing and making an etiologic diagnosis of syncope is a difficult problem and even after investigations a significant number of patients still remain unexplained.
A detailed history is of paramount importance in the evaluation of syncope. Because all evaluation is usually retrospective. We will discuss in this article an approach to syncope and how to make a probable diagnosis from history.

STEPS IN THE EVALUATION OF SYNCOPE:
Patients present with the complain of loss of consciousness. From here we have to proceed in a systematic fashion to make a diagnosis. We will approach syncope under two headings
1. Taking the history of the episode
2. Analysing the history to reach at a diagnosis

RECORDING THE HISTORY OF SYNCOPE:

Below is a sample questionnaire for recording the history
WHAT WERE THE CIRCUMSTANCES JUST PRIOR TO THE ATTACK?

• The physical position of the patient is important. Inquire whether the patient was supine, sitting or standing.

• Activity related to syncope episode (rest. change in posture, during or after exercise, during or immediately after urination, defecation cough, or swallowing)
• Predisposing factors (e.g. crowded or warm places, prolonged standing. post-prandial period) and of precipitating events (e.g. fear, intense pain, neck movements)

HOW THE ATTACK STARTED ?
• Nausea, vomiting, abdominal discomfort, feeling of cold, sweating, aura, pain in neck or shoulders, blurred vision, dizziness
• Palpitations

QUESTIONS ABOUT THE ATTACK (EYEWITNESS)
• Way of falling (slumping or kneeling over), skin color (pallor, cyanosis, flushing), duration of loss of consciousness, breathing pattern (snoring) movements (tonic, clonic, tonic-clonic, minimal myoclonus or automatism), duration of movements, onset of movement in relation to fall, tongue biting
HOW THE ATTACK ENDED?
• Nausea, vomiting, sweating, feeling of cold, confusion, muscle aches, skin color, injury, chest pain, palpitations, urinary or fecal incontinence
BACKGROUND HISTORY OF THE PATIENT
• Family history of sudden death, congenital arrhythmogenic heart disease or fainting
• Previous cardiac disease
• Neurological history (Parkinsonism, epilepsy, narcolepsy)
• Metabolic disorders (diabetes, etc.)
• Medication (antihypertensive, antianginal, antidepressant agent, antiarrhythmic, diuretics, and QT-prolonging agents) or other drugs including alcohol
• In the case of recurrent syncope, information on recurrences such as the time from the first synopal episode and on the number of spells

ANALYSIS OF HISTORY
Once the history is recorded, the next step is to differentiate syncope from other causes of transient loss of consciousness.
Causes of transient loss of consciousness (T-LOC)

1. Syncope – we will discuss
2. Neurologic or cerebrovascular disease – e.g. seizure, posterior circulation TIA
3. Metabolic syndromes and coma – e.g. hypoglycaemia, drug or alcohol intoxication, hypoxia, hypocapnea
4. Psychogenic syncope- anxiety disorders, panic disorders, somatization disorders
DIFFERENTIATING SYNCOPE FROM OTHER CAUSES OF T-LOC
Following questions help in differentiating syncope from other causes of T-LOC
(1) Did the patient experience a complete loss of consciousness?
(2) Was the loss of consciousness transient with rapid onset and short duration?
(3) Did the patient recover spontaneously, completely, and without sequelae?
(4) Did the patient lose postural tone?
If the answer to one or more of these questions is negative, other nonsyncopal causes (as listed above) of transient loss of consciousness should be evaluated.
ESTABLISHING THE CAUSE OF SYNCOPE
Features of some of the common causes of syncope

Neutrally mediated syncope Arrhythmia Seizure Psychogenic
EpidemiologyAnd clinical setting Female>malesYounger age (<55)Frequent episodes(>2)

Prolonged standing, extreme emotions, hot humid surrounding

 

Structural heart diseaseMales>femalesOlder age (>55 years)

Lesser episodes(<3)

In supine position or during exertion

Family history of sudden cardiac death

Younger age (<45yrs)Any clinical situation Females>malesOccurs in others presenceYoung age (<40 yrs)

Many episodes (many episodes in a day)

No definite trigger

 

Premonitory symptoms Longer duration(>5s)PalpitationsBlurred vision

Nausea

Warmth

Diaphoresis

Light-headedness

Shorter duration(<6s)Palpitation less common Sudden onsetBrief aura (déjà vu, olfactory, gustatory, visual Usually absent
During the episode Pallor & diaphoresisDilated pupilHypotension

Bradycardia

Urine and fecal incontinence

Brief clonic movements may occur

 

Cyanosed not paleIncontinenceClonic movements may occur Cyanosed, no pallorTongue bitingFrothing at mouth

Prolonged syncope(>5 mins)

Hypertension

Tachycardia

Horizontal eye deviations

Tonic-clonic movements

Normal colourNormal pulse and BPProlonged duration

No incontinence

Eyes closed

Residual symptoms CommonFatigueOriented Residual symptoms uncommon (unless prolonged unconsciousness) CommonMuscle achesDisorientation

Fatigue

Headache

Slow recovery

uncommon

 

Salient features of syncope due to less common causes

Cause of syncope Salient features
  1. Vascular steal syndromes (subclavian steal syndrome)

 

 

Syncope in association with symptoms of brain stem ischemia (i.e.,diplopia,tinnitus,focal weakness or sensory loss, vertigo, dysarthria.
  1. Migraine associated syncope
Throbbing unilateral headache, scintillating scotomata, nausea, vomiting, photophobia, phonophobia
  1. Orthostatic hypotension
History of orthostatic symptoms and syncope, features of autonomic failure and other neurological symptoms (e.g.,parkinsonism, disturbances of bowel, bladder , thermoregulatory and sexual function, ataxia)-volume depletion-drug and alcohol induced
  1. Carotid sinus hypersensitivity
Common in elderly, relationship to specific neck positions (neck collar, shaving etc.), carotid sinus massage reproduces symptoms or bradycardia
  1. Situational syncope
Related to specific situations ( cough, defecation, laugh, swallow, after food, sneeze, micturition etc.)
  1. Glossopharyngeal syncope
Associated with glossopharyngeal neuralgia

 

These tables provide enough information to help in diagnosis. Clinical history and physical examination has around 25% sensitivity for etiologic diagnosis of syncope. Most of these patients need further evaluation.

Special note for students about to appear in exams:
Remember the structural heart diseases which result in syncope. Important ones
1. LVOTO- aortic stenosis, HCM, coarctation of aorta
2. RVOTO – pulmonary stenosis
3. Pulmonary hypertension
4. Atrial myxoma
These conditions will have a lot of other cardiac symptoms which will help in making a clinical diagnosis. You will have to remember the natural history of important structural heart diseases and exam cases.

This article is part of the series about history taking in cardiology and is intended primarily for medical students. Physicians and practitioners are referred to ESC guideline on evaluation and management of syncope (http://www.escardio.org/guidelines-surveys/esc-guidelines/guidelinesdocuments/guidelines-syncope-ft.pdf).

Keywords : history taking in cardiology, medical students, syncope, symptoms of heart disease, analysis of symptoms

Renal artery denervation in post-stenting patients

RENAL ARTERY DENERVATION FOR HYPERTENSION REFRACTORY TO STENTING

A new study published in Journal of endovascular therapy (2014;21:181–190) has evaluated the efficacy of renal denervation therapy for hypertension refractory to renal artery stenting.

The study included ten patients (6 women; mean age 70.0±5.1 years) with an office systolic blood pressure >160 mmHg despite taking ≥3 antihypertensive drugs and uni- or bilateral renal artery stenting. These patients were treated with RDN. Radiofrequency (RF) energy was delivered to the native segment of the artery keeping a 5-mm safe distance from the stented segments. Standardized office and ambulatory blood pressure measurements, medication, and renal assessment, including renal duplex ultrasound and renal function, were determined at baseline and on follow-up to 12 months.

 

Office BP  (systolic/diastolic) at baseline was 190.0±20.4 / 84.2±10.1 mmHg. It decreased to 171.1±28.7 / 82.2±8.7, 165.5±28.4 / 76.1±7.4, and 158.3±14.2/ 75.5±9.5 mmHg (p<0.01) at 3, 6, and 12 months after RDN, respectively. Average ambulatory BP (systolic/diastolic) after 6 and 12 months decreased by −7.6/ −3.1 and −11.3 / −5.1 mmHg (p<0.05).

There was no renal artery (re)stenosis, dissection, or aneurysm within 12 months.

Creatinine, cystatin C, and glomerular filtration rate remained unchanged.

Urine albumin excretion decreased in 4/10 patients.

Renal resistive indices improved in native, but not in stented renal arteries within the follow-up period.

RF-based RDN can be safely and effectively delivered in patients with resistant hypertension and previous renal artery stenting.”

EARLY STENT THROMBOSIS

EARLY STENT THROMBOSIS- AN AUTOPSY STUDY OF LESION CHARACTERISTICS
According to a study published online ahead of print in the Journal of American college of cardiology ,patients with acute coronary syndromes (ACS) undergoing percutaneous coronary intervention (PCI) face increased risk of early stent thrombosis in the presence of high thrombus burden with certain pathological traits or suboptimal stenting.

Researchers evaluated 67 stented coronary lesions from 59 patients who presented with ACS and died within 30 days of implantation (between 2004 and 2012).

Early stent thrombosis was identified in 37 lesions from 34 patients (58%), all of whom died of stent-related causes. Of 25 patients without stent thrombosis, cause of death was stent-related in 3 (distal dissection, coronary perforation, and side branch occlusion secondary to stenting). ECG readings at the time of diagnosis revealed STEMI in 16 patients and NSTEMI in 13 patients.

All 33 patients for whom pathological information on the myocardium was available had MI on histologic examination. 

Lesion Characteristics Implicated 

No differences emerged between lesions with (n = 37) or without (n = 30) stent thrombosis in terms of stent location in the coronary tree, duration of the implant, stent type (BMS vs DES or among DES types), number of stents or total stented length, or the underlying pathological findings (eg, plaque rupture, erosion, or calcified nodule).

However, in the stented segment, the maximum index thrombus thickness at the site of greatest thrombus burden was larger and necrotic core prolapse and occlusive thrombus in the side branch were more common in thrombotic lesions compared with patent lesions. Stenting in a false lumen secondary to medial dissection was numerically higher in thrombotic lesions (table 1).

Table 1. Lesion Characteristics: Thrombosis vs Patent

  Thrombosis
(n = 37 lesions)
Patent
(n = 30 lesions)
P Value
Maximum Index Thrombus Thickness, mm 0.22 0.07 0.001
Necrotic Core Prolapse 70% 43% 0.045
Side Branch Occlusion 22% 3% 0.035
False Lumen Stenting 8% 0 0.25


In nonstented segments proximal and distal to the stented segments, severe stenosis (> 75% cross-sectional narrowing), necrotic core prolapse, and medial dissection were more common in thrombotic than patent lesions, but the differences did not reach statistical significance.

 

Comparison of culprit and nonculprit sections within lesions showed that the extent of necrotic core prolapse, medial tear, and incomplete apposition was higher in sections with thrombus.

 

In particular, independent predictors of stent thrombosis on multivariate analysis were:

  • Maximum depth of strut penetration (OR 2.3; 95% CI 1.3-4.3; P = 0.006)
  • Percentage of struts with medial tear (OR 1.8; 95% CI 1.3-2.4; P = 0.001)
  • Percentage of struts with incomplete apposition (OR 1.8; 95% CI 1.4-2.4; P < 0.001)

In addition, plaque rupture was more common in arterial sections with vs without stent thrombosis (OR 2.2; 95% CI 1.5-3.2; P < 0.001).

 

 

Careful Technique, Improved Stent Designs May Help

 

The findings emphasize the potential role of intracoronary imaging in describing the underlying plaque, quantifying the lesion extent, and assessing procedural results in terms of stent apposition.

 

Improvements in stent design may help reduce stent thrombosis risk.

 

Finally, the contribution of thrombus burden to the development of stent thrombosis reinforces the importance of potent antiplatelet and anticoagulant strategies

 

 

Study Details

 

Age, sex, indication for PCI, and past medical history were similar between subjects with and without stent thrombosis.

 

 Sources:

 

1. Nakano M, Yahagi K, Otsuka F, et al. Causes of early stent thrombosis in patients with acute coronary syndrome: an ex vivohuman autopsy study. J Am Coll Cardiol. 2014;Epub ahead of print.

2. Windecker S, O’Sullivan CJ. Mitigating the risk of early stent thrombosis [editial]. J Am Coll Cardiol. 2014;Epub ahead of prin